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ATP + a protein
ADP + a phosphoprotein
ATP + BcSak1
ADP + phosphorylated BcSak1
ATP + c-Jun N-terminal kinase
ADP + phosphorylated c-Jun N-terminal kinase
ATP + casein
ADP + phosphorylated casein
-
-
-
?
ATP + ERK
ADP + phospho-ERK
-
-
-
-
?
ATP + ERK
ADP + phosphorylated ERK
ATP + Erk-1 gene product
ADP + phosphorylated Erk-1 gene product
phosphorylation primarily on a tyrosine residue and, to a lesser extent, on a threonine
-
?
ATP + ERK1
ADP + phosphorylated ERK1
ATP + ERK1/2
ADP + phosphorylated ERK1/2
-
-
-
-
?
ATP + ERK2
ADP + phosphorylated ERK2
ATP + extracellular regulated kinase 1
ADP + phosphorylated extracellular regulated kinase 1
-
-
-
?
ATP + extracellular regulated kinase 2
ADP + phosphorylated extracellular regulated kinase 2
-
-
-
?
ATP + GhMPK7
ADP + phosphorylated GhMPK7
-
-
-
?
ATP + Janus kinase 2
ADP + phospho-Janus kinase 2
-
activation
-
-
?
ATP + JNK
ADP + JNK phosphate
ATP + JNK
ADP + phopsho-JNK
the enzyme is involved in stress-activated MAP kinase pathways, tumorigenesis, and cancer acting as a metastasis suppressor, overview
-
-
?
ATP + JNK
ADP + phospho-JNK
ATP + JNK
ADP + phosphorylated JNK
ATP + JNK1
ADP + phosphorylated JNK1
ATP + K52R-[ERK2]
ADP + phospho-K52R-[ERK2]
catalytically inactive ERK2 in which lysine-52 is substituted with arginine
-
-
?
ATP + K53M-[p38alpha]
ADP + phospho-K53M-[p38alpha]
catalytically inactive p38alpha in which lysine-53 is substituted with methionine
-
-
?
ATP + KIMPK3
ADP + phosphorylated KIMPK3
-
-
-
-
?
ATP + KIMPK6
ADP + phosphorylated KIMPK6
-
-
-
-
?
ATP + MAP kinase
ADP + phosphorylated MAP kinase
ATP + MAP kinase 6
ADP + phosphorylated Map kinase 6
Arabidopsis thaliana MAP kinase MPK6
-
-
?
ATP + MAP kinase ERK1
ADP + ?
-
-
-
?
ATP + MAPK
ADP + phosphorylated MAPK
ATP + MKK10
ADP + phosphorylated MKK10
-
-
-
?
ATP + MKK4
ADP + phosphorylated MKK4
-
-
-
?
ATP + MKP3
ADP + phosphorylated MKP3
-
-
-
?
ATP + MKP7
ADP + phosphorylated MKP7
-
-
-
?
ATP + MPK-7
ADP + phospho-MPK-7
ATP + myelin basic protein
ADP + phoshorylated myelin basic protein
-
-
-
?
ATP + myelin basic protein
ADP + phosphorylated myelin basic protein
ATP + myelin basic protein kinase
ADP + phosphorylated myelin basic protein kinase
-
-
-
?
ATP + MyoD
ADP + phospharylated MyoD
ATP + p38
ADP + ?
-
-
-
?
ATP + p38
ADP + p38 phosphate
ATP + p38
ADP + phospho-p38
ATP + p38
ADP + phosphorylated p38
-
-
-
-
?
ATP + p38 MAP kinase
ADP + ?
phosphorylates and activates p38 MAP kinase
-
-
?
ATP + p38/MPK2 kinase
ADP + ?
phosphorylates and specifically activates the p38/MPK2 subgroup of the mitogen-activated protein kinase superfamily
-
-
?
ATP + p38alpha
ADP + phosphorylated p38alpha
MKK6 phosphorylates p38 MAPK on Thr180 and Tyr182, the sites of phosphorylation that activate p38 MAPK
-
-
?
ATP + p42 MAP kinase
ADP + ?
-
-
-
?
ATP + Pfmap2
ADP + phosphorylated Pfmap2
-
the enzyme phosphorylates its potential in vivo Pfmap2 substrate largely on Thr290
-
-
?
ATP + poly-(Tyr-Glu)
ADP + phospho-poly-(Tyr-Glu)
-
tyrosine kinase substrate
-
-
?
ATP + protein
ADP + phosphoprotein
ATP + Red1
ADP + phospho-Red1
-
substrate of Mek1
-
-
?
ATP + Smad3
ADP + phosphorylated Smad3
ATP + VdHog1
ADP + phosphorylated VdHog1
ATP + [ERK2 substrate peptide]
ADP + [ERK2 substrate peptide] phosphate
MEK1
-
-
?
ATP + [myelin basic protein substrate peptide]
ADP + [myelin basic protein substrate peptide] phosphate
-
-
-
?
additional information
?
-
ATP + a protein
ADP + a phosphoprotein
-
-
-
-
?
ATP + a protein
ADP + a phosphoprotein
-
-
-
-
?
ATP + a protein
ADP + a phosphoprotein
-
MKK1 phosphorylates and activates the MAP kinases ERK1 and ERK2
-
-
?
ATP + a protein
ADP + a phosphoprotein
-
-
-
?
ATP + a protein
ADP + a phosphoprotein
-
-
-
?
ATP + a protein
ADP + a phosphoprotein
-
-
-
-
?
ATP + a protein
ADP + a phosphoprotein
-
-
-
-
?
ATP + a protein
ADP + a phosphoprotein
-
-
-
-
?
ATP + BcSak1
ADP + phosphorylated BcSak1
-
-
-
?
ATP + BcSak1
ADP + phosphorylated BcSak1
protei BcSAK1 is the putative downstream component of BOS5
-
-
?
ATP + BcSak1
ADP + phosphorylated BcSak1
-
-
-
?
ATP + BcSak1
ADP + phosphorylated BcSak1
protei BcSAK1 is the putative downstream component of BOS5
-
-
?
ATP + c-Jun N-terminal kinase
ADP + phosphorylated c-Jun N-terminal kinase
JNK activation
-
-
?
ATP + c-Jun N-terminal kinase
ADP + phosphorylated c-Jun N-terminal kinase
JNK activation
-
-
?
ATP + ERK
ADP + phosphorylated ERK
-
ERK phosphorylation by MEK1/2
-
-
?
ATP + ERK
ADP + phosphorylated ERK
-
phosphorylation by MEK activates ERK, which plays a role in pain induction modulating the A-type currents of potassium channels in neurons, ERK plays a central role in nocireceptive sensitization in the spinal cord
-
-
?
ATP + ERK
ADP + phosphorylated ERK
-
ERK phosphorylation by MEK
-
-
?
ATP + ERK1
ADP + phosphorylated ERK1
MEK2 protein stimulates Thr and Tyr phosphorylation on ERK1 and concomitantly activates ERK1 kinase activity more than 100-fold
-
-
?
ATP + ERK1
ADP + phosphorylated ERK1
phosphorylation of extracellular signal-regulated kinase 1
-
-
?
ATP + ERK2
ADP + phosphorylated ERK2
-
-
-
?
ATP + ERK2
ADP + phosphorylated ERK2
phosphorylation of extracellular signal-regulated kinase 2
-
-
?
ATP + ERK2
ADP + phosphorylated ERK2
MEK1 is able to effectively phosphorylate Thr183 and Tyr185 in the activation loop of ERK2
-
-
?
ATP + JNK
ADP + JNK phosphate
the enzyme is involved in stress-activated MAP kinase pathways, tumorigenesis, and cancer, physiologic effects, overview
-
-
?
ATP + JNK
ADP + JNK phosphate
substrate of MKK4 and MKK7 in a synergistic manner
-
-
?
ATP + JNK
ADP + phospho-JNK
the enzyme is involved in stress-activated MAP kinase pathways, tumorigenesis, and cancer, physiologic effects, overview
-
-
?
ATP + JNK
ADP + phospho-JNK
substrate of MKK4 and MKK7 in a synergistic manner
-
-
?
ATP + JNK
ADP + phospho-JNK
the enzyme is involved in stress-activated MAP kinase pathways, tumorigenesis, and cancer acting as a metastasis suppressor, overview
-
-
?
ATP + JNK
ADP + phospho-JNK
substrate of MKK4 and MKK7 in a synergistic manner
-
-
?
ATP + JNK
ADP + phospho-JNK
-
the enzyme is involved in stress-activated MAP kinase pathways and tumorigenesis, overview
-
-
?
ATP + JNK
ADP + phospho-JNK
-
substrate of MKK4 and MKK7 in a synergistic manner
-
-
?
ATP + JNK
ADP + phosphorylated JNK
-
-
-
?
ATP + JNK
ADP + phosphorylated JNK
phosphorylation of JNK at the Thr residue located in the activation loop
-
-
?
ATP + JNK
ADP + phosphorylated JNK
phosphorylation of JNK at the Tyr residue located in the activation loop
-
-
?
ATP + JNK1
ADP + phosphorylated JNK1
-
-
-
?
ATP + JNK1
ADP + phosphorylated JNK1
slight phosphorylation, JNK1 may not be the optimal substrate for the isoform
-
-
?
ATP + MAP kinase
ADP + phosphorylated MAP kinase
activation of MAP kinase
-
-
?
ATP + MAP kinase
ADP + phosphorylated MAP kinase
the enzyme is involved in the mitogen-activated protein kinase signaling pathway important for e.g. flagellar length control, the enzyme is involved in differentiation of the parasite and is important for virulence and infection of human peritoneal macrophages
-
-
?
ATP + MAP kinase
ADP + phosphorylated MAP kinase
docking site for the substrate is located close to the N-terminal Lys4 and consists of 2 basic amino acid residues separated by a spacer of 2-6 variable residues from an L/I/V-X-L/I/V sequence
-
-
?
ATP + MAP kinase
ADP + phosphorylated MAP kinase
-
-
-
?
ATP + MAPK
ADP + phosphorylated MAPK
-
MAPK activation
-
-
?
ATP + MAPK
ADP + phosphorylated MAPK
-
-
-
-
?
ATP + MPK-7
ADP + phospho-MPK-7
-
-
-
-
?
ATP + MPK-7
ADP + phospho-MPK-7
-
MKK3 interacts with MPK7 in planta
-
-
?
ATP + MPK-7
ADP + phospho-MPK-7
-
-
-
-
?
ATP + MPK-7
ADP + phospho-MPK-7
-
MKK3 interacts with MPK7 in planta
-
-
?
ATP + myelin basic protein
ADP + phosphorylated myelin basic protein
-
-
-
?
ATP + myelin basic protein
ADP + phosphorylated myelin basic protein
-
Pfnek3 phosphorylates MBP on threonine, but not serine residues
-
-
?
ATP + MyoD
ADP + phospharylated MyoD
phosphorylation at Tyr156, activated MEK1 associates with MyoD
-
-
?
ATP + MyoD
ADP + phospharylated MyoD
phosphorylation at Tyr156 recombinant GST-tagged MyoD substrate. Mutational analysis of phosphorylation sites using MyoD Tyr mutants, overview
-
-
?
ATP + p38
ADP + p38 phosphate
the enzyme is involved in stress-activated MAP kinase pathways, tumorigenesis, and cancer, physiologic effects, overview
-
-
?
ATP + p38
ADP + p38 phosphate
substrate of MKK7
-
-
?
ATP + p38
ADP + phospho-p38
-
-
-
-
?
ATP + p38
ADP + phospho-p38
the enzyme is involved in stress-activated MAP kinase pathways, tumorigenesis, and cancer, physiologic effects, overview
-
-
?
ATP + p38
ADP + phospho-p38
substrate of MKK4
-
-
?
ATP + p38
ADP + phospho-p38
the enzyme is involved in stress-activated MAP kinase pathways, tumorigenesis, and cancer acting as a metastasis suppressor, overview
-
-
?
ATP + p38
ADP + phospho-p38
substrate of MKK4
-
-
?
ATP + p38
ADP + phospho-p38
substrate of MKK7
-
-
?
ATP + p38
ADP + phospho-p38
-
the enzyme is involved in stress-activated MAP kinase pathways and tumorigenesis, overview
-
-
?
ATP + p38
ADP + phospho-p38
-
substrate of MKK4 and MKK7
-
-
?
ATP + p38
ADP + phospho-p38
activation by phosphorylation
-
-
?
ATP + p38
ADP + phospho-p38
signal cascade upstream activation by phosphorylation, sorbitol induced activation of p38 in salmon TO cells does not require MKK6a, b or c
-
-
?
ATP + protein
ADP + phosphoprotein
mek-2 acts between lin-45 raf and sur-1/mpk-1 in a signal transduction pathway used in the control of vulval differentiation and other developmental events
-
-
?
ATP + protein
ADP + phosphoprotein
Hst7 activates the mating pathway even in the absence of upstream signaling components including the Ste7 regulator Ste11, elevates the basal level of the pheromone-inducible FUS1 gene, and amplifies the pseudohyphal growth response in diploid cells
-
-
?
ATP + protein
ADP + phosphoprotein
the enzyme functions in a novel Drosophila MAPK pathway, controlling puckered expression and morphogenetic activity of the dorsal epidermis
-
-
?
ATP + protein
ADP + phosphoprotein
the enzyme is involved in the mitogenic growth factor signal transduction pathway in vertebrates
-
-
?
ATP + protein
ADP + phosphoprotein
-
-
-
?
ATP + protein
ADP + phosphoprotein
enzyme is involved in independent human MAP-kinase signal transduction pathway
-
-
?
ATP + protein
ADP + phosphoprotein
MKK4 may participate in a tumor suppressive signaling pathway distinct from DPC4, p16, p53, and BRCA2. The enzyme is a component of a stress and cytokine-induced signal transduction pathway involving MAPK proteins, additional role for MKK4 in tumor suppression
-
-
?
ATP + protein
ADP + phosphoprotein
the enzyme is an activator of the c-Jun NH2-terminal kinase, the enzyme is a component of the JNK signal transduction pathway
-
-
?
ATP + protein
ADP + phosphoprotein
enzyme is the major activator for p38
-
-
?
ATP + protein
ADP + phosphoprotein
enzyme is involved on MAPK signal transduction pathway
-
-
?
ATP + protein
ADP + phosphoprotein
the enzyme is the major activator of RK/p38
-
-
?
ATP + protein
ADP + phosphoprotein
MEKK3 regulates the SAPK and the ERK pathway directly
-
-
?
ATP + protein
ADP + phosphoprotein
ASK1 may be a key element in the mechanism of stress-induced and cytokine-induced apoptosis
-
-
?
ATP + protein
ADP + phosphoprotein
MEK6 is a member of the p38 kinase cascade and efficiently phosphorylates p38, induces phosphorylation of ATF2 by p38 but does not phosphorylate ATF2 directly
-
-
?
ATP + protein
ADP + phosphoprotein
MAPKKK5 may be an upstream activator of MKK4 in the c-Jun N-terminal kinase pathway
-
-
?
ATP + protein
ADP + phosphoprotein
sequences located in the N-terminus of MEK5 may be important in coupling GTPase signaling molecules to the MEK5 protein kinase cascade
-
-
?
ATP + protein
ADP + phosphoprotein
phosphorylates kinase-inactive Erk-1 protein primarily on a tyrosine residue and, to a lesser extent, on a threonine
-
-
?
ATP + protein
ADP + phosphoprotein
possible role for ASK1 in tissue development during embryogenesis as well as cytokine-induced apoptosis
-
-
?
ATP + protein
ADP + phosphoprotein
enzyme is the major activator for p38
-
-
?
ATP + protein
ADP + phosphoprotein
enzyme is involved on MAPK signal transduction pathway
-
-
?
ATP + protein
ADP + phosphoprotein
MEKK 2 preferentially activates JNK
-
-
?
ATP + protein
ADP + phosphoprotein
MEKK 3 preferentially activates p42/44MAPK
-
-
?
ATP + protein
ADP + phosphoprotein
-
-
-
?
ATP + protein
ADP + phosphoprotein
tyrosine/threonine kinase
-
-
?
ATP + protein
ADP + phosphoprotein
the enzyme renders the cell resistant to polymyxin B
-
-
?
ATP + protein
ADP + phosphoprotein
MKK1 and MKK2 function in a signal transduction pathway involving the protein kinases encoded by PKC1, BCK1, and MPK1. The site of action for MKK1 and MKK2 is between BCK1 and MPK1
-
-
?
ATP + protein
ADP + phosphoprotein
enzyme is involved in the response of haploid yeast cells to peptide mating pheromones
-
-
?
ATP + protein
ADP + phosphoprotein
Pek1, in its unphosphorylated form, acts as a potent negative regulator of Pmk1 MAPK signalling. Mkh1, an upstream MAPKK kinase, converts Pek1 from being an inhibitor to an activator. Pek1 has a dual stimulatory and inhibitory function which depends on its phosphorylation state
-
-
?
ATP + protein
ADP + phosphoprotein
enzyme plays a key role in initiation of septum formation and cytokinesis in fission yeast, p120cdc7 interacts with the cdc11 protein in the control of septation
-
-
?
ATP + protein
ADP + phosphoprotein
dosage-dependent regulator of mitosis in Schizosaccharomyces pombe
-
-
?
ATP + protein
ADP + phosphoprotein
Spg1p is a key element in controlling the onset of septum formation that acts through the Cdc7p kinase
-
-
?
ATP + protein
ADP + phosphoprotein
byr1 is an important gene in the sexual differentiation pathway and at least part of ras1 function is to act directly or indirectly through byr1 to modulate protein phosphorylation
-
-
?
ATP + protein
ADP + phosphoprotein
the enzyme is a component of the mkh1 signaling pathway. Mkh1, Skh1 and Spm1 constitute a MAPK cascade in Schizosaccharomyces pombe
-
-
?
ATP + protein
ADP + phosphoprotein
the enzyme is required for locus-dependent and locus-independent steps in the fungal life cycle. Necessary for locus-dependent processes, such as conjugation tube formation, filament formation, and maintenance of filamentous growth, and for locus-independent processes, such as tumor induction and teliospore germination
-
-
?
ATP + protein
ADP + phosphoprotein
the enzyme undergoes autophosphorylation on Ser, Thr and Tyr
-
-
?
ATP + protein
ADP + phosphoprotein
the enzyme functions as a direct upstream activator for a presumed MAP kinase homolog in each signal transduction pathway involved in the regulation of cell cycle progression or cellular responses to extracellular signals
-
-
?
ATP + Smad3
ADP + phosphorylated Smad3
-
-
-
-
?
ATP + Smad3
ADP + phosphorylated Smad3
-
mitogen-activated protein kinase kinase-1 regulates SMAD3 expression in epithelial and smooth muscle cells, which is stimulated by TGFbeta-1, SMAD3 is a transcription factor that mediates TGF-?1 signaling and is important in many of the cellular processes that regulate fibrosis and inflammation, overview
-
-
?
ATP + VdHog1
ADP + phosphorylated VdHog1
-
VdHog1 is a mitogen-activated protein kinase, MAPK
-
-
?
ATP + VdHog1
ADP + phosphorylated VdHog1
-
VdHog1 is a mitogen-activated protein kinase, MAPK
-
-
?
additional information
?
-
Arabidopsis thaliana mitogen-activated protein kinase kinase MKK1 is implicated in biotic and abiotic stress responses as part of a signaling cascade including MEKK1 and MPK4, MKK1 and MKK2 function upstream of MPK4, overview. The mkk1/2 double mutant is similar to the mpk4 mutant, as both: (1) are dark green dwarves with curled leaves, (2) constitutively overproduce salicylic acid and exhibit enhanced resistance to biotrophic pathogens and insensitivity to JA, and (3) have enhanced basal expression of PR1 and other SA-dependent defense genes
-
-
?
additional information
?
-
Arabidopsis thaliana mitogen-activated protein kinase kinase MKK1 is implicated in biotic and abiotic stress responses as part of a signaling cascade including MEKK1 and MPK4, MKK1 and MKK2 function upstream of MPK4, overview. The mkk1/2 double mutant is similar to the mpk4 mutant, as both: (1) are dark green dwarves with curled leaves, (2) constitutively overproduce salicylic acid and exhibit enhanced resistance to biotrophic pathogens and insensitivity to JA, and (3) have enhanced basal expression of PR1 and other SA-dependent defense genes
-
-
?
additional information
?
-
Arabidopsis thaliana mitogen-activated protein kinase kinase MKK2 is implicated in biotic and abiotic stress responses as part of a signaling cascade including MEKK1 and MPK4, MKK1 and MKK2 function upstream of MPK4, overview. mkk2 single mutants appear morphologically normal, the mkk1/2 double mutant is similar to the mpk4 mutant, as both: (1) are dark green dwarves with curled leaves, (2) constitutively overproduce salicylic acid and exhibit enhanced resistance to biotrophic pathogens and insensitivity to JA, and (3) have enhanced basal expression of PR1 and other SA-dependent defense genes
-
-
?
additional information
?
-
Arabidopsis thaliana mitogen-activated protein kinase kinase MKK2 is implicated in biotic and abiotic stress responses as part of a signaling cascade including MEKK1 and MPK4, MKK1 and MKK2 function upstream of MPK4, overview. mkk2 single mutants appear morphologically normal, the mkk1/2 double mutant is similar to the mpk4 mutant, as both: (1) are dark green dwarves with curled leaves, (2) constitutively overproduce salicylic acid and exhibit enhanced resistance to biotrophic pathogens and insensitivity to JA, and (3) have enhanced basal expression of PR1 and other SA-dependent defense genes
-
-
?
additional information
?
-
-
MKK3 positively regulates PR gene expression and plays a role in defense against Pst DC3000. MKK3 is an upstream activator of the group C MAPKs MPK1, MPK2, MPK7, and MPK14, overview
-
-
?
additional information
?
-
-
MKK3 positively regulates PR gene expression and plays a role in defense against Pst DC3000. MKK3 is an upstream activator of the group C MAPKs MPK1, MPK2, MPK7, and MPK14, overview
-
-
?
additional information
?
-
-
substrate binding via the D-domain of the MKK
-
-
?
additional information
?
-
-
enzyme is part of mitogen-activated protein kinase pathways, crosstalk and regulation mechanism, overview
-
-
?
additional information
?
-
GhMKK3 interacts with GhMPK7, a typical C group MAPK member, and GhPIP1 potein. GhMPK7 is phosphorylated by GhMKK3 in protoplasts
-
-
?
additional information
?
-
-
GhMKK3 interacts with GhMPK7, a typical C group MAPK member, and GhPIP1 potein. GhMPK7 is phosphorylated by GhMKK3 in protoplasts
-
-
?
additional information
?
-
MEKK3 activates SEK and MEK, the known kinases targeting SAPK and ERK respectively
-
-
?
additional information
?
-
-
MEKK3 activates SEK and MEK, the known kinases targeting SAPK and ERK respectively
-
-
?
additional information
?
-
-
MEK1/2 are involved in the mitogen-activated protein kinase signaling pathway and in cancer tumorigenesis
-
-
?
additional information
?
-
-
the enzyme is involved in the mitogen-activated protein kinase signaling pathway, which is linked to the cell cycle machinery, constitutive phosphorylation and activation of the enzyme leads to cell proliferation in choroidal melanoma cells
-
-
?
additional information
?
-
MKK7gamma1 is unable to phosphorylate p38
-
-
?
additional information
?
-
-
MKK7gamma1 is unable to phosphorylate p38
-
-
?
additional information
?
-
-
mitogen-activated protein kinase kinase signaling promotes growth and vascularization of fibrosarcoma it is required for growth of fibrosarcoma-derived xenografts, to maintain tumor blood flow, and for vascularization of fibrosarcoma-derived xenografts, and MKK signaling is required for the release of proangiogenic factors from other sarcoma-derived cell lines, overview
-
-
?
additional information
?
-
-
pro-oncogenic role of mitogen-activated protein kinase kinase 4 in cancer, overview
-
-
?
additional information
?
-
pro-oncogenic role of mitogen-activated protein kinase kinase 4 in cancer, overview
-
-
?
additional information
?
-
pro-oncogenic role of mitogen-activated protein kinase kinase 4 in cancer, overview
-
-
?
additional information
?
-
-
the MEKK-1 is involved in stress-induced cell death of insulin-producing cells and essential in JNK activation, overview
-
-
?
additional information
?
-
-
TNF-alpha receptor signaling regulates epithelial cell secretion of inflammation and invasion mediators involving signaling through IkappaB kinase complex 2, IKB, nuclear factor kappaB, extracellular signal-regulated kinase, mitogen-activated protein kinase kinase, p38, and phosphatidylinositol 3-kinase, and Akt1/2. MEK, p38, and IKK inhibitors block TNF-alpha-induced IL-8, IL-6, and GM-CSF secretion and 12z invasion, whereas the PI3K inhibitors do not, overview
-
-
?
additional information
?
-
-
MKK signaling is required for cell proliferation and for cytokine release in vitro
-
-
?
additional information
?
-
-
substrate binding via the D-domain of the MKK
-
-
?
additional information
?
-
substrate binding via the D-domain of the MKK
-
-
?
additional information
?
-
substrate binding via the D-domain of the MKK
-
-
?
additional information
?
-
development of a continuous spectrophotometric assay for mitogen-activated protein kinase kinases. The assay relies on the measurement of phosphoprotein product generated in the first step of the MAPK kinase reaction. Dephosphorylation of the phosphoprotein is coupled to a MAPK phosphatase, MKP3, to generate phosphate, which is then used as the substrate of purine nucleoside phosphorylase to catalyze the N-glycosidic cleavage of 2-amino 6-mercapto 7-methyl purine ribonucleoside. Of the reaction products ribose 1-phosphate and 2-amino 6-mercapto 7-methylpurine, the latter has a high absorbance at 360 nm relative to the nucleoside and, hence, provides a spectrophotometric signal that can be continuously followed. In the presence of excess phosphatase, the phosphorylated protein substrate molecules undergo dephosphorylation almost immediately after their formation. The steady-state use of the resultant inorganic phosphate is a reflection of the constant initial velocity of the exchange reaction. Method development and evaluation, overview
-
-
?
additional information
?
-
development of a continuous spectrophotometric assay for mitogen-activated protein kinase kinases. The assay relies on the measurement of phosphoprotein product generated in the first step of the MAPK kinase reaction. Dephosphorylation of the phosphoprotein is coupled to a MAPK phosphatase, MKP3, to generate phosphate, which is then used as the substrate of purine nucleoside phosphorylase to catalyze the N-glycosidic cleavage of 2-amino 6-mercapto 7-methyl purine ribonucleoside. Of the reaction products ribose 1-phosphate and 2-amino 6-mercapto 7-methylpurine, the latter has a high absorbance at 360 nm relative to the nucleoside and, hence, provides a spectrophotometric signal that can be continuously followed. In the presence of excess phosphatase, the phosphorylated protein substrate molecules undergo dephosphorylation almost immediately after their formation. The steady-state use of the resultant inorganic phosphate is a reflection of the constant initial velocity of the exchange reaction. Method development and evaluation, overview
-
-
?
additional information
?
-
development of a continuous spectrophotometric assay for mitogen-activated protein kinase kinases. The assay relies on the measurement of phosphoprotein product generated in the first step of the MAPK kinase reaction. Dephosphorylation of the phosphoprotein is coupled to a MAPK phosphatase, MKP5, to generate phosphate, which is then used as the substrate of purine nucleoside phosphorylase to catalyze the N-glycosidic cleavage of 2-amino 6-mercapto 7-methyl purine ribonucleoside. Of the reaction products ribose 1-phosphate and 2-amino 6-mercapto 7-methylpurine, the latter has a high absorbance at 360 nm relative to the nucleoside and, hence, provides a spectrophotometric signal that can be continuously followed. In the presence of excess phosphatase, the phosphorylated protein substrate molecules undergo dephosphorylation almost immediately after their formation. The steady-state use of the resultant inorganic phosphate is a reflection of the constant initial velocity of the exchange reaction. Method development and evaluation, overview
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-
?
additional information
?
-
development of a continuous spectrophotometric assay for mitogen-activated protein kinase kinases. The assay relies on the measurement of phosphoprotein product generated in the first step of the MAPK kinase reaction. Dephosphorylation of the phosphoprotein is coupled to a MAPK phosphatase, MKP5, to generate phosphate, which is then used as the substrate of purine nucleoside phosphorylase to catalyze the N-glycosidic cleavage of 2-amino 6-mercapto 7-methyl purine ribonucleoside. Of the reaction products ribose 1-phosphate and 2-amino 6-mercapto 7-methylpurine, the latter has a high absorbance at 360 nm relative to the nucleoside and, hence, provides a spectrophotometric signal that can be continuously followed. In the presence of excess phosphatase, the phosphorylated protein substrate molecules undergo dephosphorylation almost immediately after their formation. The steady-state use of the resultant inorganic phosphate is a reflection of the constant initial velocity of the exchange reaction. Method development and evaluation, overview
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?
additional information
?
-
the enzyme performs autophosphorylation
-
-
?
additional information
?
-
-
the enzyme performs autophosphorylation
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-
?
additional information
?
-
-
the enzyme is involved in the mitogen-activated protein kinase signaling pathway regulating cell dissociation of cancer cells, MEK2 is an invasion-metastasis related factor between highly and weakly invasive cells, occludin acts as antagonist
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-
?
additional information
?
-
-
the enzyme is involved in the mitogen-activated protein kinase signaling pathway, which is involved in e.g. formalin-induced inflammatory pain and thermal hyperalgesia, overview
-
-
?
additional information
?
-
-
pro-oncogenic role of mitogen-activated protein kinase kinase 4 in cancer, overview. MKK4 is also involved in the immune system and development of B- and T-cells, as well as in cardiac hypertrophy, overview
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-
?
additional information
?
-
pro-oncogenic role of mitogen-activated protein kinase kinase 4 in cancer, overview. MKK4 is also involved in the immune system and development of B- and T-cells, as well as in cardiac hypertrophy, overview
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-
?
additional information
?
-
pro-oncogenic role of mitogen-activated protein kinase kinase 4 in cancer, overview. MKK4 is also involved in the immune system and development of B- and T-cells, as well as in cardiac hypertrophy, overview
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-
?
additional information
?
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-
substrate binding via the D-domain of the MKK
-
-
?
additional information
?
-
substrate binding via the D-domain of the MKK
-
-
?
additional information
?
-
substrate binding via the D-domain of the MKK
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-
?
additional information
?
-
MKK4 phosphorylates JNK on Tyr, while MKK7 phosphorylates Thr, and MKK4 and MKK7 together cause dual phosphorylation of JNK thus, optimal activation
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-
?
additional information
?
-
MKK4 phosphorylates JNK on Tyr, while MKK7 phosphorylates Thr, and MKK4 and MKK7 together cause dual phosphorylation of JNK thus, optimal activation
-
-
?
additional information
?
-
MAP kinase kinase 1 is regulated by salt and drought stresses, differential expression, overview
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-
?
additional information
?
-
MAP kinase kinase 1 is regulated by salt and drought stresses, differential expression, overview
-
-
?
additional information
?
-
MAP kinase kinase 1 is regulated by salt and drought stresses, differential expression, overview
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-
?
additional information
?
-
MAP kinase kinase 1 is regulated by salt and drought stresses, differential expression, overview
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-
?
additional information
?
-
MAP kinase kinase 1 is regulated by salt and drought stresses, differential expression, overview
-
-
?
additional information
?
-
-
MAP kinase kinase 1 is regulated by salt and drought stresses, differential expression, overview
-
-
?
additional information
?
-
MAP kinase kinase 10-2 is regulated only by cold stress, differential expression, overview
-
-
?
additional information
?
-
MAP kinase kinase 10-2 is regulated only by cold stress, differential expression, overview
-
-
?
additional information
?
-
MAP kinase kinase 10-2 is regulated only by cold stress, differential expression, overview
-
-
?
additional information
?
-
MAP kinase kinase 10-2 is regulated only by cold stress, differential expression, overview
-
-
?
additional information
?
-
MAP kinase kinase 10-2 is regulated only by cold stress, differential expression, overview
-
-
?
additional information
?
-
-
MAP kinase kinase 10-2 is regulated only by cold stress, differential expression, overview
-
-
?
additional information
?
-
MAP kinase kinase 6 is strongly regulated by cold and salt stresses, differential expression, overview
-
-
?
additional information
?
-
MAP kinase kinase 6 is strongly regulated by cold and salt stresses, differential expression, overview
-
-
?
additional information
?
-
MAP kinase kinase 6 is strongly regulated by cold and salt stresses, differential expression, overview
-
-
?
additional information
?
-
MAP kinase kinase 6 is strongly regulated by cold and salt stresses, differential expression, overview
-
-
?
additional information
?
-
MAP kinase kinase 6 is strongly regulated by cold and salt stresses, differential expression, overview
-
-
?
additional information
?
-
-
MAP kinase kinase 6 is strongly regulated by cold and salt stresses, differential expression, overview
-
-
?
additional information
?
-
MAP kinase kinases 4 is strongly regulated by cold and salt stresses, differential expression, overview
-
-
?
additional information
?
-
MAP kinase kinases 4 is strongly regulated by cold and salt stresses, differential expression, overview
-
-
?
additional information
?
-
MAP kinase kinases 4 is strongly regulated by cold and salt stresses, differential expression, overview
-
-
?
additional information
?
-
MAP kinase kinases 4 is strongly regulated by cold and salt stresses, differential expression, overview
-
-
?
additional information
?
-
MAP kinase kinases 4 is strongly regulated by cold and salt stresses, differential expression, overview
-
-
?
additional information
?
-
-
MAP kinase kinases 4 is strongly regulated by cold and salt stresses, differential expression, overview
-
-
?
additional information
?
-
regulation and differential expression, overview
-
-
?
additional information
?
-
regulation and differential expression, overview
-
-
?
additional information
?
-
regulation and differential expression, overview
-
-
?
additional information
?
-
regulation and differential expression, overview
-
-
?
additional information
?
-
regulation and differential expression, overview
-
-
?
additional information
?
-
-
regulation and differential expression, overview
-
-
?
additional information
?
-
protein-protein docking of MAPKK and MAPK
-
-
?
additional information
?
-
protein-protein docking of MAPKK and MAPK
-
-
?
additional information
?
-
protein-protein docking of MAPKK and MAPK
-
-
?
additional information
?
-
protein-protein docking of MAPKK and MAPK
-
-
?
additional information
?
-
protein-protein docking of MAPKK and MAPK
-
-
?
additional information
?
-
-
the enzyme displays both serine/threonine and tyrosine kinase activities in autophosphorylation reactions as well as in phosphorylation of the exogenous myelin basic protein substrate. Ability of Pfnek3 to autophosphorylate on both the serine/threonine and the tyrosine residues. The dual-specificity activity of the kinase is distinctly influenced by the type of divalent cation present
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-
?
additional information
?
-
-
the enzyme is involved in the mitogen-activated protein kinase signaling pathway
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-
?
additional information
?
-
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the enzyme is involved in the mitogen-activated protein kinase signaling pathway, pathway induction by neurotrophin stabilizes the axonal growth cone, pathway inhibitor semaphorin 3F induces growth cone collaps in sympathetic neurons and reduction of axonal growth
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?
additional information
?
-
-
the enzyme is involved in the mitogen-activated protein kinase signaling pathway, which is involved in e.g. activation of Egr-1 and subsequently of c-Fos and cyclin D1 after mechanic injury for induction/regulation of regrowth of smooth vascular cells, vascular smooth muscle cell proliferation plays an important role in pathogenesis of atherosclerosis and post-angioplasty restenosis, overview
-
-
?
additional information
?
-
-
adenosine-stimulated adrenal steroidogenesis involves the adenosine A2A and A2B receptors and the Janus kinase 2-mitogen-activated protein kinase kinase-extracellular signal-regulated kinase signaling pathway, overview
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-
?
additional information
?
-
-
lithium protection of phencyclidine-induced neurotoxicity and cell death in developing brain: the role of phosphatidylinositol-3 kinase/Akt and mitogen-activated protein kinase kinase/extracellular signal-regulated kinase signaling pathways, overview
-
-
?
additional information
?
-
-
role of mitogen-activated protein kinase kinase 4 in cancer, overview. MKK4 is also involved in the immune system and development of B- and T-cells, as well as in cardiac hypertrophy, overview
-
-
?
additional information
?
-
-
substrate binding via the D-domain of the MKK
-
-
?
additional information
?
-
-
-
-
?
additional information
?
-
Pek1, in its unphosphorylated form, acts as a potent negative regulator of Pmk1 MAPK signalling. Mkh1, an upstream MAPKK kinase, converts Pek1 from being an inhibitor to an activator. Pek1 has a dual stimulatory and inhibitory function which depends on its phosphorylation state
-
-
?
additional information
?
-
-
Pek1, in its unphosphorylated form, acts as a potent negative regulator of Pmk1 MAPK signalling. Mkh1, an upstream MAPKK kinase, converts Pek1 from being an inhibitor to an activator. Pek1 has a dual stimulatory and inhibitory function which depends on its phosphorylation state
-
-
?
additional information
?
-
-
substrate binding via the D-domain of the MKK
-
-
?
additional information
?
-
interaction of ZmMKK1 and ZmMEKK1, a MAP kinase kinase kinase, in vitro
-
-
?
additional information
?
-
-
interaction of ZmMKK1 and ZmMEKK1, a MAP kinase kinase kinase, in vitro
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?
Please wait a moment until the data is sorted. This message will disappear when the data is sorted.
ATP + a protein
ADP + a phosphoprotein
ATP + BcSak1
ADP + phosphorylated BcSak1
ATP + c-Jun N-terminal kinase
ADP + phosphorylated c-Jun N-terminal kinase
ATP + ERK
ADP + phospho-ERK
-
-
-
-
?
ATP + ERK
ADP + phosphorylated ERK
ATP + ERK1
ADP + phosphorylated ERK1
phosphorylation of extracellular signal-regulated kinase 1
-
-
?
ATP + ERK1/2
ADP + phosphorylated ERK1/2
-
-
-
-
?
ATP + ERK2
ADP + phosphorylated ERK2
ATP + extracellular regulated kinase 1
ADP + phosphorylated extracellular regulated kinase 1
-
-
-
?
ATP + extracellular regulated kinase 2
ADP + phosphorylated extracellular regulated kinase 2
-
-
-
?
ATP + GhMPK7
ADP + phosphorylated GhMPK7
-
-
-
?
ATP + Janus kinase 2
ADP + phospho-Janus kinase 2
-
activation
-
-
?
ATP + JNK
ADP + JNK phosphate
the enzyme is involved in stress-activated MAP kinase pathways, tumorigenesis, and cancer, physiologic effects, overview
-
-
?
ATP + JNK
ADP + phopsho-JNK
the enzyme is involved in stress-activated MAP kinase pathways, tumorigenesis, and cancer acting as a metastasis suppressor, overview
-
-
?
ATP + JNK
ADP + phospho-JNK
ATP + JNK
ADP + phosphorylated JNK
ATP + MAP kinase
ADP + phosphorylated MAP kinase
ATP + MAPK
ADP + phosphorylated MAPK
ATP + MPK-7
ADP + phospho-MPK-7
ATP + myelin basic protein
ADP + phosphorylated myelin basic protein
-
Pfnek3 phosphorylates MBP on threonine, but not serine residues
-
-
?
ATP + MyoD
ADP + phospharylated MyoD
phosphorylation at Tyr156, activated MEK1 associates with MyoD
-
-
?
ATP + p38
ADP + p38 phosphate
the enzyme is involved in stress-activated MAP kinase pathways, tumorigenesis, and cancer, physiologic effects, overview
-
-
?
ATP + p38
ADP + phospho-p38
ATP + p38alpha
ADP + phosphorylated p38alpha
MKK6 phosphorylates p38 MAPK on Thr180 and Tyr182, the sites of phosphorylation that activate p38 MAPK
-
-
?
ATP + Pfmap2
ADP + phosphorylated Pfmap2
-
the enzyme phosphorylates its potential in vivo Pfmap2 substrate largely on Thr290
-
-
?
ATP + protein
ADP + phosphoprotein
ATP + Smad3
ADP + phosphorylated Smad3
-
mitogen-activated protein kinase kinase-1 regulates SMAD3 expression in epithelial and smooth muscle cells, which is stimulated by TGFbeta-1, SMAD3 is a transcription factor that mediates TGF-?1 signaling and is important in many of the cellular processes that regulate fibrosis and inflammation, overview
-
-
?
ATP + VdHog1
ADP + phosphorylated VdHog1
additional information
?
-
ATP + a protein
ADP + a phosphoprotein
-
-
-
-
?
ATP + a protein
ADP + a phosphoprotein
-
-
-
-
?
ATP + a protein
ADP + a phosphoprotein
-
-
-
?
ATP + a protein
ADP + a phosphoprotein
-
-
-
?
ATP + a protein
ADP + a phosphoprotein
-
-
-
-
?
ATP + a protein
ADP + a phosphoprotein
-
-
-
-
?
ATP + a protein
ADP + a phosphoprotein
-
-
-
-
?
ATP + BcSak1
ADP + phosphorylated BcSak1
-
-
-
?
ATP + BcSak1
ADP + phosphorylated BcSak1
-
-
-
?
ATP + c-Jun N-terminal kinase
ADP + phosphorylated c-Jun N-terminal kinase
JNK activation
-
-
?
ATP + c-Jun N-terminal kinase
ADP + phosphorylated c-Jun N-terminal kinase
JNK activation
-
-
?
ATP + ERK
ADP + phosphorylated ERK
-
ERK phosphorylation by MEK1/2
-
-
?
ATP + ERK
ADP + phosphorylated ERK
-
phosphorylation by MEK activates ERK, which plays a role in pain induction modulating the A-type currents of potassium channels in neurons, ERK plays a central role in nocireceptive sensitization in the spinal cord
-
-
?
ATP + ERK2
ADP + phosphorylated ERK2
-
-
-
?
ATP + ERK2
ADP + phosphorylated ERK2
phosphorylation of extracellular signal-regulated kinase 2
-
-
?
ATP + JNK
ADP + phospho-JNK
the enzyme is involved in stress-activated MAP kinase pathways, tumorigenesis, and cancer, physiologic effects, overview
-
-
?
ATP + JNK
ADP + phospho-JNK
the enzyme is involved in stress-activated MAP kinase pathways, tumorigenesis, and cancer acting as a metastasis suppressor, overview
-
-
?
ATP + JNK
ADP + phospho-JNK
-
the enzyme is involved in stress-activated MAP kinase pathways and tumorigenesis, overview
-
-
?
ATP + JNK
ADP + phosphorylated JNK
phosphorylation of JNK at the Thr residue located in the activation loop
-
-
?
ATP + JNK
ADP + phosphorylated JNK
phosphorylation of JNK at the Tyr residue located in the activation loop
-
-
?
ATP + MAP kinase
ADP + phosphorylated MAP kinase
activation of MAP kinase
-
-
?
ATP + MAP kinase
ADP + phosphorylated MAP kinase
the enzyme is involved in the mitogen-activated protein kinase signaling pathway important for e.g. flagellar length control, the enzyme is involved in differentiation of the parasite and is important for virulence and infection of human peritoneal macrophages
-
-
?
ATP + MAPK
ADP + phosphorylated MAPK
-
MAPK activation
-
-
?
ATP + MAPK
ADP + phosphorylated MAPK
-
-
-
-
?
ATP + MPK-7
ADP + phospho-MPK-7
-
MKK3 interacts with MPK7 in planta
-
-
?
ATP + MPK-7
ADP + phospho-MPK-7
-
MKK3 interacts with MPK7 in planta
-
-
?
ATP + p38
ADP + phospho-p38
-
-
-
-
?
ATP + p38
ADP + phospho-p38
the enzyme is involved in stress-activated MAP kinase pathways, tumorigenesis, and cancer, physiologic effects, overview
-
-
?
ATP + p38
ADP + phospho-p38
the enzyme is involved in stress-activated MAP kinase pathways, tumorigenesis, and cancer acting as a metastasis suppressor, overview
-
-
?
ATP + p38
ADP + phospho-p38
-
the enzyme is involved in stress-activated MAP kinase pathways and tumorigenesis, overview
-
-
?
ATP + p38
ADP + phospho-p38
signal cascade upstream activation by phosphorylation, sorbitol induced activation of p38 in salmon TO cells does not require MKK6a, b or c
-
-
?
ATP + protein
ADP + phosphoprotein
mek-2 acts between lin-45 raf and sur-1/mpk-1 in a signal transduction pathway used in the control of vulval differentiation and other developmental events
-
-
?
ATP + protein
ADP + phosphoprotein
Hst7 activates the mating pathway even in the absence of upstream signaling components including the Ste7 regulator Ste11, elevates the basal level of the pheromone-inducible FUS1 gene, and amplifies the pseudohyphal growth response in diploid cells
-
-
?
ATP + protein
ADP + phosphoprotein
the enzyme functions in a novel Drosophila MAPK pathway, controlling puckered expression and morphogenetic activity of the dorsal epidermis
-
-
?
ATP + protein
ADP + phosphoprotein
the enzyme is involved in the mitogenic growth factor signal transduction pathway in vertebrates
-
-
?
ATP + protein
ADP + phosphoprotein
-
-
-
?
ATP + protein
ADP + phosphoprotein
enzyme is involved in independent human MAP-kinase signal transduction pathway
-
-
?
ATP + protein
ADP + phosphoprotein
MKK4 may participate in a tumor suppressive signaling pathway distinct from DPC4, p16, p53, and BRCA2. The enzyme is a component of a stress and cytokine-induced signal transduction pathway involving MAPK proteins, additional role for MKK4 in tumor suppression
-
-
?
ATP + protein
ADP + phosphoprotein
the enzyme is an activator of the c-Jun NH2-terminal kinase, the enzyme is a component of the JNK signal transduction pathway
-
-
?
ATP + protein
ADP + phosphoprotein
enzyme is the major activator for p38
-
-
?
ATP + protein
ADP + phosphoprotein
enzyme is involved on MAPK signal transduction pathway
-
-
?
ATP + protein
ADP + phosphoprotein
the enzyme is the major activator of RK/p38
-
-
?
ATP + protein
ADP + phosphoprotein
MEKK3 regulates the SAPK and the ERK pathway directly
-
-
?
ATP + protein
ADP + phosphoprotein
ASK1 may be a key element in the mechanism of stress-induced and cytokine-induced apoptosis
-
-
?
ATP + protein
ADP + phosphoprotein
MEK6 is a member of the p38 kinase cascade and efficiently phosphorylates p38, induces phosphorylation of ATF2 by p38 but does not phosphorylate ATF2 directly
-
-
?
ATP + protein
ADP + phosphoprotein
MAPKKK5 may be an upstream activator of MKK4 in the c-Jun N-terminal kinase pathway
-
-
?
ATP + protein
ADP + phosphoprotein
sequences located in the N-terminus of MEK5 may be important in coupling GTPase signaling molecules to the MEK5 protein kinase cascade
-
-
?
ATP + protein
ADP + phosphoprotein
possible role for ASK1 in tissue development during embryogenesis as well as cytokine-induced apoptosis
-
-
?
ATP + protein
ADP + phosphoprotein
enzyme is the major activator for p38
-
-
?
ATP + protein
ADP + phosphoprotein
enzyme is involved on MAPK signal transduction pathway
-
-
?
ATP + protein
ADP + phosphoprotein
MEKK 2 preferentially activates JNK
-
-
?
ATP + protein
ADP + phosphoprotein
MEKK 3 preferentially activates p42/44MAPK
-
-
?
ATP + protein
ADP + phosphoprotein
-
-
-
?
ATP + protein
ADP + phosphoprotein
the enzyme renders the cell resistant to polymyxin B
-
-
?
ATP + protein
ADP + phosphoprotein
MKK1 and MKK2 function in a signal transduction pathway involving the protein kinases encoded by PKC1, BCK1, and MPK1. The site of action for MKK1 and MKK2 is between BCK1 and MPK1
-
-
?
ATP + protein
ADP + phosphoprotein
enzyme is involved in the response of haploid yeast cells to peptide mating pheromones
-
-
?
ATP + protein
ADP + phosphoprotein
Pek1, in its unphosphorylated form, acts as a potent negative regulator of Pmk1 MAPK signalling. Mkh1, an upstream MAPKK kinase, converts Pek1 from being an inhibitor to an activator. Pek1 has a dual stimulatory and inhibitory function which depends on its phosphorylation state
-
-
?
ATP + protein
ADP + phosphoprotein
enzyme plays a key role in initiation of septum formation and cytokinesis in fission yeast, p120cdc7 interacts with the cdc11 protein in the control of septation
-
-
?
ATP + protein
ADP + phosphoprotein
dosage-dependent regulator of mitosis in Schizosaccharomyces pombe
-
-
?
ATP + protein
ADP + phosphoprotein
Spg1p is a key element in controlling the onset of septum formation that acts through the Cdc7p kinase
-
-
?
ATP + protein
ADP + phosphoprotein
byr1 is an important gene in the sexual differentiation pathway and at least part of ras1 function is to act directly or indirectly through byr1 to modulate protein phosphorylation
-
-
?
ATP + protein
ADP + phosphoprotein
the enzyme is a component of the mkh1 signaling pathway. Mkh1, Skh1 and Spm1 constitute a MAPK cascade in Schizosaccharomyces pombe
-
-
?
ATP + protein
ADP + phosphoprotein
the enzyme is required for locus-dependent and locus-independent steps in the fungal life cycle. Necessary for locus-dependent processes, such as conjugation tube formation, filament formation, and maintenance of filamentous growth, and for locus-independent processes, such as tumor induction and teliospore germination
-
-
?
ATP + protein
ADP + phosphoprotein
the enzyme functions as a direct upstream activator for a presumed MAP kinase homolog in each signal transduction pathway involved in the regulation of cell cycle progression or cellular responses to extracellular signals
-
-
?
ATP + VdHog1
ADP + phosphorylated VdHog1
-
VdHog1 is a mitogen-activated protein kinase, MAPK
-
-
?
ATP + VdHog1
ADP + phosphorylated VdHog1
-
VdHog1 is a mitogen-activated protein kinase, MAPK
-
-
?
additional information
?
-
Arabidopsis thaliana mitogen-activated protein kinase kinase MKK1 is implicated in biotic and abiotic stress responses as part of a signaling cascade including MEKK1 and MPK4, MKK1 and MKK2 function upstream of MPK4, overview. The mkk1/2 double mutant is similar to the mpk4 mutant, as both: (1) are dark green dwarves with curled leaves, (2) constitutively overproduce salicylic acid and exhibit enhanced resistance to biotrophic pathogens and insensitivity to JA, and (3) have enhanced basal expression of PR1 and other SA-dependent defense genes
-
-
?
additional information
?
-
Arabidopsis thaliana mitogen-activated protein kinase kinase MKK1 is implicated in biotic and abiotic stress responses as part of a signaling cascade including MEKK1 and MPK4, MKK1 and MKK2 function upstream of MPK4, overview. The mkk1/2 double mutant is similar to the mpk4 mutant, as both: (1) are dark green dwarves with curled leaves, (2) constitutively overproduce salicylic acid and exhibit enhanced resistance to biotrophic pathogens and insensitivity to JA, and (3) have enhanced basal expression of PR1 and other SA-dependent defense genes
-
-
?
additional information
?
-
Arabidopsis thaliana mitogen-activated protein kinase kinase MKK2 is implicated in biotic and abiotic stress responses as part of a signaling cascade including MEKK1 and MPK4, MKK1 and MKK2 function upstream of MPK4, overview. mkk2 single mutants appear morphologically normal, the mkk1/2 double mutant is similar to the mpk4 mutant, as both: (1) are dark green dwarves with curled leaves, (2) constitutively overproduce salicylic acid and exhibit enhanced resistance to biotrophic pathogens and insensitivity to JA, and (3) have enhanced basal expression of PR1 and other SA-dependent defense genes
-
-
?
additional information
?
-
Arabidopsis thaliana mitogen-activated protein kinase kinase MKK2 is implicated in biotic and abiotic stress responses as part of a signaling cascade including MEKK1 and MPK4, MKK1 and MKK2 function upstream of MPK4, overview. mkk2 single mutants appear morphologically normal, the mkk1/2 double mutant is similar to the mpk4 mutant, as both: (1) are dark green dwarves with curled leaves, (2) constitutively overproduce salicylic acid and exhibit enhanced resistance to biotrophic pathogens and insensitivity to JA, and (3) have enhanced basal expression of PR1 and other SA-dependent defense genes
-
-
?
additional information
?
-
-
MKK3 positively regulates PR gene expression and plays a role in defense against Pst DC3000. MKK3 is an upstream activator of the group C MAPKs MPK1, MPK2, MPK7, and MPK14, overview
-
-
?
additional information
?
-
-
MKK3 positively regulates PR gene expression and plays a role in defense against Pst DC3000. MKK3 is an upstream activator of the group C MAPKs MPK1, MPK2, MPK7, and MPK14, overview
-
-
?
additional information
?
-
-
enzyme is part of mitogen-activated protein kinase pathways, crosstalk and regulation mechanism, overview
-
-
?
additional information
?
-
GhMKK3 interacts with GhMPK7, a typical C group MAPK member, and GhPIP1 potein. GhMPK7 is phosphorylated by GhMKK3 in protoplasts
-
-
?
additional information
?
-
-
GhMKK3 interacts with GhMPK7, a typical C group MAPK member, and GhPIP1 potein. GhMPK7 is phosphorylated by GhMKK3 in protoplasts
-
-
?
additional information
?
-
-
MEK1/2 are involved in the mitogen-activated protein kinase signaling pathway and in cancer tumorigenesis
-
-
?
additional information
?
-
-
the enzyme is involved in the mitogen-activated protein kinase signaling pathway, which is linked to the cell cycle machinery, constitutive phosphorylation and activation of the enzyme leads to cell proliferation in choroidal melanoma cells
-
-
?
additional information
?
-
-
mitogen-activated protein kinase kinase signaling promotes growth and vascularization of fibrosarcoma it is required for growth of fibrosarcoma-derived xenografts, to maintain tumor blood flow, and for vascularization of fibrosarcoma-derived xenografts, and MKK signaling is required for the release of proangiogenic factors from other sarcoma-derived cell lines, overview
-
-
?
additional information
?
-
-
pro-oncogenic role of mitogen-activated protein kinase kinase 4 in cancer, overview
-
-
?
additional information
?
-
pro-oncogenic role of mitogen-activated protein kinase kinase 4 in cancer, overview
-
-
?
additional information
?
-
pro-oncogenic role of mitogen-activated protein kinase kinase 4 in cancer, overview
-
-
?
additional information
?
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-
the MEKK-1 is involved in stress-induced cell death of insulin-producing cells and essential in JNK activation, overview
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-
?
additional information
?
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TNF-alpha receptor signaling regulates epithelial cell secretion of inflammation and invasion mediators involving signaling through IkappaB kinase complex 2, IKB, nuclear factor kappaB, extracellular signal-regulated kinase, mitogen-activated protein kinase kinase, p38, and phosphatidylinositol 3-kinase, and Akt1/2. MEK, p38, and IKK inhibitors block TNF-alpha-induced IL-8, IL-6, and GM-CSF secretion and 12z invasion, whereas the PI3K inhibitors do not, overview
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-
?
additional information
?
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the enzyme is involved in the mitogen-activated protein kinase signaling pathway regulating cell dissociation of cancer cells, MEK2 is an invasion-metastasis related factor between highly and weakly invasive cells, occludin acts as antagonist
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?
additional information
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the enzyme is involved in the mitogen-activated protein kinase signaling pathway, which is involved in e.g. formalin-induced inflammatory pain and thermal hyperalgesia, overview
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-
?
additional information
?
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pro-oncogenic role of mitogen-activated protein kinase kinase 4 in cancer, overview. MKK4 is also involved in the immune system and development of B- and T-cells, as well as in cardiac hypertrophy, overview
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-
?
additional information
?
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pro-oncogenic role of mitogen-activated protein kinase kinase 4 in cancer, overview. MKK4 is also involved in the immune system and development of B- and T-cells, as well as in cardiac hypertrophy, overview
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-
?
additional information
?
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pro-oncogenic role of mitogen-activated protein kinase kinase 4 in cancer, overview. MKK4 is also involved in the immune system and development of B- and T-cells, as well as in cardiac hypertrophy, overview
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-
?
additional information
?
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MKK4 phosphorylates JNK on Tyr, while MKK7 phosphorylates Thr, and MKK4 and MKK7 together cause dual phosphorylation of JNK thus, optimal activation
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-
?
additional information
?
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MKK4 phosphorylates JNK on Tyr, while MKK7 phosphorylates Thr, and MKK4 and MKK7 together cause dual phosphorylation of JNK thus, optimal activation
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-
?
additional information
?
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MAP kinase kinase 1 is regulated by salt and drought stresses, differential expression, overview
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-
?
additional information
?
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MAP kinase kinase 1 is regulated by salt and drought stresses, differential expression, overview
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-
?
additional information
?
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MAP kinase kinase 1 is regulated by salt and drought stresses, differential expression, overview
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-
?
additional information
?
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MAP kinase kinase 1 is regulated by salt and drought stresses, differential expression, overview
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-
?
additional information
?
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MAP kinase kinase 1 is regulated by salt and drought stresses, differential expression, overview
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?
additional information
?
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MAP kinase kinase 1 is regulated by salt and drought stresses, differential expression, overview
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?
additional information
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MAP kinase kinase 10-2 is regulated only by cold stress, differential expression, overview
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?
additional information
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MAP kinase kinase 10-2 is regulated only by cold stress, differential expression, overview
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-
?
additional information
?
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MAP kinase kinase 10-2 is regulated only by cold stress, differential expression, overview
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?
additional information
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MAP kinase kinase 10-2 is regulated only by cold stress, differential expression, overview
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?
additional information
?
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MAP kinase kinase 10-2 is regulated only by cold stress, differential expression, overview
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-
?
additional information
?
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MAP kinase kinase 10-2 is regulated only by cold stress, differential expression, overview
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?
additional information
?
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MAP kinase kinase 6 is strongly regulated by cold and salt stresses, differential expression, overview
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?
additional information
?
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MAP kinase kinase 6 is strongly regulated by cold and salt stresses, differential expression, overview
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-
?
additional information
?
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MAP kinase kinase 6 is strongly regulated by cold and salt stresses, differential expression, overview
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-
?
additional information
?
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MAP kinase kinase 6 is strongly regulated by cold and salt stresses, differential expression, overview
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?
additional information
?
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MAP kinase kinase 6 is strongly regulated by cold and salt stresses, differential expression, overview
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?
additional information
?
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MAP kinase kinase 6 is strongly regulated by cold and salt stresses, differential expression, overview
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-
?
additional information
?
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MAP kinase kinases 4 is strongly regulated by cold and salt stresses, differential expression, overview
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-
?
additional information
?
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MAP kinase kinases 4 is strongly regulated by cold and salt stresses, differential expression, overview
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-
?
additional information
?
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MAP kinase kinases 4 is strongly regulated by cold and salt stresses, differential expression, overview
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-
?
additional information
?
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MAP kinase kinases 4 is strongly regulated by cold and salt stresses, differential expression, overview
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-
?
additional information
?
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MAP kinase kinases 4 is strongly regulated by cold and salt stresses, differential expression, overview
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-
?
additional information
?
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MAP kinase kinases 4 is strongly regulated by cold and salt stresses, differential expression, overview
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-
?
additional information
?
-
regulation and differential expression, overview
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-
?
additional information
?
-
regulation and differential expression, overview
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-
?
additional information
?
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regulation and differential expression, overview
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-
?
additional information
?
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regulation and differential expression, overview
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-
?
additional information
?
-
regulation and differential expression, overview
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-
?
additional information
?
-
-
regulation and differential expression, overview
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-
?
additional information
?
-
protein-protein docking of MAPKK and MAPK
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-
?
additional information
?
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protein-protein docking of MAPKK and MAPK
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-
?
additional information
?
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protein-protein docking of MAPKK and MAPK
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-
?
additional information
?
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protein-protein docking of MAPKK and MAPK
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-
?
additional information
?
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protein-protein docking of MAPKK and MAPK
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?
additional information
?
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the enzyme is involved in the mitogen-activated protein kinase signaling pathway
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?
additional information
?
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the enzyme is involved in the mitogen-activated protein kinase signaling pathway, pathway induction by neurotrophin stabilizes the axonal growth cone, pathway inhibitor semaphorin 3F induces growth cone collaps in sympathetic neurons and reduction of axonal growth
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?
additional information
?
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the enzyme is involved in the mitogen-activated protein kinase signaling pathway, which is involved in e.g. activation of Egr-1 and subsequently of c-Fos and cyclin D1 after mechanic injury for induction/regulation of regrowth of smooth vascular cells, vascular smooth muscle cell proliferation plays an important role in pathogenesis of atherosclerosis and post-angioplasty restenosis, overview
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-
?
additional information
?
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adenosine-stimulated adrenal steroidogenesis involves the adenosine A2A and A2B receptors and the Janus kinase 2-mitogen-activated protein kinase kinase-extracellular signal-regulated kinase signaling pathway, overview
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-
?
additional information
?
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lithium protection of phencyclidine-induced neurotoxicity and cell death in developing brain: the role of phosphatidylinositol-3 kinase/Akt and mitogen-activated protein kinase kinase/extracellular signal-regulated kinase signaling pathways, overview
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?
additional information
?
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role of mitogen-activated protein kinase kinase 4 in cancer, overview. MKK4 is also involved in the immune system and development of B- and T-cells, as well as in cardiac hypertrophy, overview
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?
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1-(2,3-dihydroxypropyl)-4-(2-fluoro-4-iodoanilino)-6-oxo-1,6-dihydro-3-pyridinecarboxamide
-
1-(3-cyanopropyl)-4-(2-fluoro-4-iodoanilino)-6-oxo-1,6-dihydro-3-pyridinecarboxamide
-
1-allyl-4-(2-fluoro-4-iodoanilino)-6-oxo-1,6-dihydro-3-pyridinecarboxamide
-
1-ethyl-4-(2-fluoro-4-iodoanilino)-6-oxo-1,6-dihydro-3-pyridinecarboxamide
-
1-methyl-4-(2-naphthylamino)-6-oxo-1,6-dihydro-3-pyridinecarboxamide
-
3,4-difluoro-2-[(2-fluoro-4-iodophenyl)amino]benzamide
-
3,4-difluoro-N-(3-{5-[(2-fluoro-4-iodophenyl)amino]-6,8-dimethyl-2,4,7-trioxo-3-phenyl-3,4,6,7-tetrahydropyrido[4,3-d]pyrimidin-1(2H)-yl}phenyl)-5-hydroxybenzamide
-
-
3,4-difluoro-N-{3-[3-(3-fluoro-4-hydroxyphenyl)-5-[(2-fluoro-4-iodophenyl)amino]-6,8-dimethyl-2,4,7-trioxo-3,4,6,7-tetrahydropyrido[4,3-d]pyrimidin-1(2H)-yl]phenyl}-5-hydroxybenzamide
-
-
3,4-difluoro-N-{3-[5-({2-fluoro-4-[(hydroxymethyl)amino]phenyl}amino)-3-(3-fluoro-4-hydroxyphenyl)-6,8-dimethyl-2,4,7-trioxo-3,4,6,7-tetrahydropyrido[4,3-d]pyrimidin-1(2H)-yl]phenyl}-5-hydroxybenzamide
-
-
3,4-difluoro-N-{3-[5-{[2-fluoro-4-(formylamino)phenyl]amino}-3-(3-fluoro-4-hydroxyphenyl)-6,8-dimethyl-2,4,7-trioxo-3,4,6,7-tetrahydropyrido[4,3-d]pyrimidin-1(2H)-yl]phenyl}-5-hydroxybenzamide
-
-
4-(2-fluoro-4-iodoanilino)-1-(2-hydroxyethyl)-6-oxo-1,6-dihydro-3-pyridinecarboxamide
-
4-(2-fluoro-4-iodoanilino)-1-(3-hydroxypropyl)-6-oxo-1,6-dihydro-3-pyridinecarboxamide
-
4-(2-fluoro-4-iodoanilino)-1-methyl-6-oxo-1,6-dihydro-3-pyridinecarboxamide
-
4-(2-fluoro-4-iodoanilino)-1-methyl-6-oxo-1,6-dihydro-3-pyridinecarboxylic acid
-
4-(2-fluoro-4-iodoanilino)-1-[2-(2-methoxyethoxy)ethyl]-6-oxo-1,6-dihydro-3-pyridinecarboxamide
-
4-(2-fluoro-4-iodoanilino)-6-oxo-1,6-dihydro-3-pyridinecarboxamide
-
4-(2-fluoro-4-iodoanilino)-6-oxo-1-propyl-1,6-dihydro-3-pyridinecarboxamide
-
4-(2-fluoro-4-iodoanilino)-N,1-dimethyl-6-oxo-1,6-dihydro-3-pyridinecarboxamide
-
4-(2-fluoro-4-iodoanilino)-N,N,1-trimethyl-6-oxo-1,6-dihydro-3-pyridinecarboxamide
-
4-(2-fluoro-4-iodoanilino)-N-(2-hydroxyethoxy)-1-methyl-6-oxo-1,6-dihydro-3-pyridinecarboxamide
-
4-(2-fluoro-4-iodoanilino)-N-(2-hydroxyethyl)-1-methyl-6-oxo-1,6-dihydro-3-pyridinecarboxamide
-
4-(2-fluoro-4-iodoanilino)-N-(3-hydroxypropyl)-1-methyl-6-oxo-1,6-dihydro-3-pyridinecarboxamide
-
4-(2-fluoro-4-methylanilino)-1-methyl-6-oxo-1,6-dihydro-3-pyridinecarboxamide
-
4-(2-fluoro-4-methylsulfanylphenylamino)-1-methyl-6-oxo-1,6-dihydro-3 -pyridinecarboxamide
-
4-(3,4-dichlorophenylamino)-1-methyl-6-oxo-1,6-dihydro-3-pyridinecarboxamide
-
4-(4-bromo-2-fluoroanilino)-1-methyl-6-oxo-1,6-dihydro-3-pyridinecarboxamide
-
4-(4-bromo-2-fluoroanilino)-N-(2-hydroxyethoxy)-1-methyl-6-oxo-1,6-dihydro-3-pyridinecarboxamide
-
4-(4-bromo-2-fluorophenylamino)-1-methylpyridin-2(1H)-one
-
selective anthranilic acid type inhibitors, residues K97, I141, M143, F129, V127, I126, L118, F209, V211, and S212 of MEK1/2 are important for interaction with the inhibitor, noncompetitive to ATP, inhibition of ERK phosphorylation by MEK1/2 by the derivatives with IC50 values of 6.8-124 nM, low cytotoxic effects, overview
4-(4-cyano-2-fluoroanilino)-1-methyl-6-oxo-1,6-dihydro-3-pyridinecarboxamide
-
4-(4-ethyl-2-fluoroanilino)-1-methyl-6-oxo-1,6-dihydro-3-pyridinecarboxamide
-
4-(4-ethynyl-2-fluoroanilino)-1-methyl-6-oxo-1,6-dihydro-3-pyridinecarboxamide
-
4-amino-1-[3,4-difluoro-2-[(2-fluoro-4-iodophenyl)amino]phenyl]-2-hydroxybutan-1-one
-
4-[2-fluoro-4-(1,1,2,2,3,3,4,4,4-nonafluorobutyl)anilino]-1-methyl-6-oxo-1,6 -dihydro-3-pyridinecarboxamide
-
4-[2-fluoro-4-(3-hydroxypropyl)anilino]-1-methyl-6-oxo-1,6-dihydro-3-pyridinecarboxamide
-
4-[3,4-difluoro-2-[(2-fluoro-4-iodophenyl)amino]phenyl]-3-hydroxy-4-oxobutanamide
-
anthrax lethal toxin
-
i.e. LeTx, inactivates MKKs, LeTx treatment reduces the levels of phosphorylated extracellular signal-regulated kinase and p38 MAPK in vitro, short treatments with LeTx only modestly affects cell proliferation, sustained treatment markedly reduces cell numbers, LeTx also substantially inhibits the extracellular release of angioproliferative factors including vascular endothelial growth factor, interleukin-8, and basic fibroblast growth factor, overview
-
AS-703026
-
a MEK12 inhibitor, binds in the allosteric site of MEK1. For A-375 cells, AS-703026 has a growth IC50 of 4 nM
BAY 869766
-
i.e. RDEA119
Berberine
-
suppresses MEK/ERK-dependent Egr-1 signaling pathway and inhibits vascular smooth muscle cell regrowth after mechanical injury in vitro
CH-4987655/RO4987655
-
a MEK1/2 inhibitor
Cocoa procyanidin B2
procyanidin B2 suppresses TPA-induced phosphorylation of MEK, ERK, and p90RSK in JB6 P+ cells, suppresses JB6 P+ cell transformation by inhibiting mitogen-activated protein kinase kinase, molecular mechanism, overview
Cocoa procyanidins
suppresses JB6 P+ cell transformation by inhibiting mitogen-activated protein kinase kinase, molecular mechanisms of the chemopreventive potential of cocoa and its active ingredients, overview
-
E6201
-
blocks proliferation of many of the cell lines typically used in testing MEK inhibitors, such as Colo205 and MiaPaca-2
ethyl 4-(2-fluoro-4-iodoanilino)-1-methyl-6-oxo-1,6-dihydro-3-pyridinecarboxylate
-
LL-Z1640-2
-
a MEK1 inhibitor, which shows reasonable MEK inhibition but a very short half-life
MIIC
i.e. MEK inhibitor I, the MEK1/2 inhibitor causes NAD(H) reduction, heme oxidation, and decreased oxygen consumption; i.e. MEK inhibitor I, the MEK1/2 inhibitor causes NAD(H) reduction, heme oxidation, and decreased oxygen consumption
N-(3-{3-cyclopropyl-5-[(2-fluoro-4-iodophenyl)amino]-6,8-dimethyl-2,4,7-trioxo-3,4,6,7-tetrahydropyrido[4,3-d]pyrimidin-1(2H)-yl}phenyl)-3,4-difluoro-5-hydroxybenzamide
-
-
N-(3-{3-cyclopropyl-5-[(2-fluoro-4-iodophenyl)amino]-6,8-dimethyl-2,4,7-trioxo-3,4,6,7-tetrahydropyrido[4,3-d]pyrimidin-1(2H)-yl}phenyl)benzamide
-
-
N-(3-{3-cyclopropyl-5-[(4-cyclopropyl-2-fluorophenyl)amino]-6,8-dimethyl-2,4,7-trioxo-3,4,6,7-tetrahydropyrido[4,3-d]pyrimidin-1(2H)-yl}phenyl)-2-oxopropanamide
-
-
N-(3-{5-[(2-fluoro-4-iodophenyl)amino]-6,8-dimethyl-2,4,7-trioxo-3-phenyl-3,4,6,7-tetrahydropyrido[4,3-d]pyrimidin-1(2H)-yl}phenyl)-2-oxopropanamide
-
-
N-(3-{5-[(2-fluoro-4-iodophenyl)amino]-6,8-dimethyl-2,4,7-trioxo-3-phenyl-3,4,6,7-tetrahydropyrido[4,3-d]pyrimidin-1(2H)-yl}phenyl)benzamide
-
-
N-{3-[3-(3-fluoro-4-hydroxyphenyl)-5-[(2-fluoro-4-iodophenyl)amino]-6,8-dimethyl-2,4,7-trioxo-3,4,6,7-tetrahydropyrido[4,3-d]pyrimidin-1(2H)-yl]phenyl}-2-oxopropanamide
-
-
N-{3-[5-(cyclopropylmethyl)-3-(3-fluoro-4-hydroxyphenyl)-6,8-dimethyl-2,4,7-trioxo-3,4,6,7-tetrahydropyrido[4,3-d]pyrimidin-1(2H)-yl]phenyl}-3,4-difluoro-5-hydroxybenzamide
-
-
N-{3-[5-(cyclopropylmethyl)-3-(4-hydroxy-3-iodophenyl)-6,8-dimethyl-2,4,7-trioxo-3,4,6,7-tetrahydropyrido[4,3-d]pyrimidin-1(2H)-yl]phenyl}-3,4-difluoro-5-hydroxybenzamide
-
-
N-{3-[5-(cyclopropylmethyl)-3-(4-hydroxyphenyl)-6,8-dimethyl-2,4,7-trioxo-3,4,6,7-tetrahydropyrido[4,3-d]pyrimidin-1(2H)-yl]phenyl}-3,4-difluoro-5-hydroxybenzamide
-
-
PD184352
a MEK-specific inhibitor
PD184352/CI-1040
-
a allosteric, non-ATP competitive MEK inhibitor
PD198306
an orally active MEK1/2 inhibitor, acting as an uncoupler; an orally active MEK1/2 inhibitor, acting as an uncoupler
phencyclidine
-
a N-methyl-D-aspartate receptor antagonist, it is neurotoxic to developing brains and results in schizophrenia-like behaviors later in development, it elicites time-dependent inhibition of the MEK/ERK and PI-3K/Akt pathways, overview
tert-butyl [5-(aminocarbonyl)-4-(2-fluoro-4-iodoanilino)-2-oxo-1(2H)-pyridinyl]acetate
-
XL-518/GDC-0973
-
selective for MEK1 relative to MEK2
ZINC00142380
i.e. 1-methyl-1H-indole-2-carboxylic acid, inhibitor obtained from virtual screening
ZINC00167997
i.e. 2-[(2-carboxyethyl)amino]benzoic acid, inhibitor obtained from virtual screening
ZINC00388545
i.e. 2,6-dihydroxybenzoic acid, inhibitor obtained from virtual screening
ZINC00389778
i.e. 2,4,6-trihydroxybenzoic acid, inhibitor obtained from virtual screening
ZINC00391412
i.e. 2,6-dihydroxy-4-methylbenzoic acid, inhibitor obtained from virtual screening
ZINC01641166
i.e. 2,4,5-trihydroxybenzoic acid, inhibitor obtained from virtual screening
ZINC02349698
i.e. 7-chloro-1H-indole-2-carboxylic acid, inhibitor obtained from virtual screening
ZINC06091752
i.e. 2,3,6-trihydroxybenzoic acid, inhibitor obtained from virtual screening
ZINC13526482
i.e. 2,5-dihydroxy-4-methylbenzoic acid, inhibitor obtained from virtual screening
ZINC14817730
i.e. (2,4,6-trihydroxyphenyl)acetic acid, inhibitor obtained from virtual screening
[5-(aminocarbonyl)-4-(2-fluoro-4-iodoanilino)-2-oxo-1(2H)-pyridinyl]acetic acid
-
AZD8330
-
-
AZD8330
-
ARRY424704, renamed AZD8330
CH4987655
-
-
CH4987655
-
or RO4987655, a non-ATP competitive inhibitor, highly selective for MEK1
CI-1040
-
-
PD318088
-
-
PD98059
-
MEK-specific inhibitor, enhances antileukemia activity of Mdm2 antagonists in AML cells and p53-mediated transcription-dependent apoptosis. MEK inhibition accumulates p53 into the nucleus in OCIAML-3 cells, but does not affect the nucleoplasmic localization of Mdm2. The inhibitor restricts p21-mediated antiapoptotic mechanisms by repressing p53-dependent induction of p21, which enables Nutlin-3a to induce sufficient apoptosis in G1-phase cells
PD98059
-
inhibition of MEK1 with either PD98059 results in a substantial dose-dependent inhibition of SMAD3 promoter activity, reduced SMAD3 protein expression in A549 cells and airway smooth muscle cells after treatment with MEK1 inhibitors; substantial dose-dependent inhibition of SMAD3 promoter activity, 5.8fold reduction, MEK1 inhibition of SMAD3 promoter function is primarily mediated through an Sp1-dependent mechanism
PD98059
the MEK1/2 inhibitor causes NAD(H) reduction, heme oxidation, and decreased oxygen consumption; the MEK1/2 inhibitor causes NAD(H) reduction, heme oxidation, and decreased oxygen consumption
PD98059
-
MAPKK inhibitor, inhibits IPO expression stimulated by staurosporine
PD98059
-
inhibitor specific for MEK/ERK activation, granulocyte/macrophage colony number is decreased by ca. 60%
PD98059
-
the MEK inhibitor completely blocks adenosine-stimulated corticosterone production
PD98059
-
MEK inhibitor, effective dose of 0.05 mM
selumetinib
-
-
selumetinib
-
i.e. AZD6244, potent and highly selective, non-ATP competitive inhibitor of MEK1/2, MEK1 phosphorylation of ERK2. The compound inhibits growth of cell lines
siRNA
-
MEK1/2-specific inhibitor, delays, but does not block the passage of synchronized HeLa cells into M phase
-
siRNA
cells transiently transfected with two independent sets of siRNAs show significant down-regulation of MKK3 and phosphorylated MKK3
-
siRNA
-
knockdown of MEK, HSCs give rise to Mac-1+ myeloid cells less efficiently than control HSCs
-
trametinib
a mitogen-activated protein kinase kinase 1 (MEK1)/MEK2 inhibitor with activity against multiple myeloid cell lines at low nanomolar concentrations, preferential activity among RAS-mutated myeloid malignancies. During clinical oral treatment, most commonly reported treatment-related adverse events are diarrhea, rash, nausea, and increased alanine aminotransferase levels, repeated cycles of trametinib are well tolerated with manageable or reversible toxicities, overview; a mitogen-activated protein kinase kinase 1 (MEK1)/MEK2 inhibitor with activity against multiple myeloid cell lines at low nanomolar concentrations, preferential activity among RAS-mutated myeloid malignancies. During clinical oral treatment, most commonly reported treatment-related adverse events are diarrhea, rash, nausea, and increased alanine aminotransferase levels, repeated cycles of trametinib are well tolerated with manageable or reversible toxicities, overview
U0126
-
inhibition of MEK1 with either UO126 results in a substantial dose-dependent inhibition of SMAD3 promoter activity, reduced SMAD3 protein expression in A549 cells and airway smooth muscle cells after treatment with MEK1 inhibitors; substantial dose-dependent inhibition of SMAD3 promoter activity, 2.3fold reduction, MEK1 inhibition of SMAD3 promoter function is primarily mediated through an Sp1-dependent mechanism
U0126
-
MEK1/2-specific inhibitor, delays, but does not block the passage of synchronized HeLa cells into M phase
U0126
-
a allosteric, non-ATP competitive MEK inhibitor
U0126
the MEK1/2 inhibitor causes NAD(H) reduction, heme oxidation, and decreased oxygen consumption; the MEK1/2 inhibitor causes NAD(H) reduction, heme oxidation, and decreased oxygen consumption
U0126
-
inhibitor specific for MEK/ERK activation, granulocyte/macrophage colony number is decreased by ca. 60%
U0126
-
specific MEK inhibitor
U0126
-
potent MEK-1/2 inhibitor, cellular size, DNA fragmentation, nuclear condensation, and the phosphorylated ERK-1 protein products of H9c2 cells treated with Porphyromonas gingivalis medium, are all significantly reduced after pre-administration of U0126
U0126
-
the MEK inhibitor completely blocks adenosine-stimulated corticosterone production
U0126
-
MEK inhibitor, effective dose at 0.1 mM
U0126
a specific inhibitor for MEK1/2/ERK1/2
additional information
-
MEK, p38, and IKK inhibitors block TNF-alpha-induced IL-8, IL-6, and GM-CSF secretion and 12z invasion, whereas the PI3K inhibitors do not
-
additional information
-
stress-induced target of rapamycin complex 1 activation can be blocked by RNAi against mitogen-activated protein kinase kinase 3 and 6
-
additional information
-
known inhibitor structure screening, and design of specific allosteric MEK1/2 inhibitors with improved pharmacokinetic/pharmacodynamic profiles to be used as alternative cancer medications. Trametinib is used as the lead structure. Molecular docking and binding simulations, thermodynamics, and quantitative structure-activity relationships, allosteric inhibitory site, overview
-
additional information
-
the MEK enzyme contains a hydrophobic allosteric pocket adjacent to the ATP-binding site which allows for the design of highly selective allosteric inhibitors
-
additional information
design of small molecule MEK1/2 inhibitors to block ERK1/2-mediated signaling and inhibit proliferation. Four structurally distinct MEK1/2 inhibitors acutely affect mitochondrial bioenergetics. The anti-mitochondrial effects of MEK1/2 inhibitors determine the proliferative potential; design of small molecule MEK1/2 inhibitors to block ERK1/2-mediated signaling and inhibit proliferation. Four structurally distinct MEK1/2 inhibitors acutely affect mitochondrial bioenergetics. The anti-mitochondrial effects of MEK1/2 inhibitors determine the proliferative potential
-
additional information
design of small molecule MEK1/2 inhibitors to block ERK1/2-mediated signaling and inhibit proliferation. Four structurally distinct MEK1/2 inhibitors acutely affect mitochondrial bioenergetics. The anti-mitochondrial effects of MEK1/2 inhibitors determine the proliferative potential; design of small molecule MEK1/2 inhibitors to block ERK1/2-mediated signaling and inhibit proliferation. Four structurally distinct MEK1/2 inhibitors acutely affect mitochondrial bioenergetics. The anti-mitochondrial effects of MEK1/2 inhibitors determine the proliferative potential
-
additional information
SymRK acts as an inhibitor of SIP2 kinase activity when MPK6 is used as a substrate, suggesting that SymRK may serve as a negative regulator of the SIP2 signaling pathway. SymRK and SIP2 interact with each other but cannot use one another as a substrate for phosphorylation. SymRK can autophosphorylate itself but fails to phosphorylate the kinase-negative SIP2-KR, suggesting that SymRK is neither a potential phosphorylation target nor a kinase source of SIP2
-
additional information
-
SymRK acts as an inhibitor of SIP2 kinase activity when MPK6 is used as a substrate, suggesting that SymRK may serve as a negative regulator of the SIP2 signaling pathway. SymRK and SIP2 interact with each other but cannot use one another as a substrate for phosphorylation. SymRK can autophosphorylate itself but fails to phosphorylate the kinase-negative SIP2-KR, suggesting that SymRK is neither a potential phosphorylation target nor a kinase source of SIP2
-
additional information
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occludin acts as antagonist of the MEK and ERK signaling pathway inducing cell aggregation of pancreatic cancer cells
-
additional information
inactivated by the serine/threonine phosphatase 2A but not by the protein-tyrosine phosphatase 1B
-
additional information
inactivated by the serine/threonine phosphatase 2A but not by the protein-tyrosine phosphatase 1B
-
additional information
-
inactivated by the serine/threonine phosphatase 2A but not by the protein-tyrosine phosphatase 1B
-
additional information
-
treatment with LY294002, paclitaxel, or serum starvation does not induce apoptosis of wild-type MEF cells
-
additional information
-
design and synthesis of 4-anilino-5-carboxamido-2-pyridone MEK1 inhibitors using a combination of medicinal chemistry, computational chemistry, and structural elucidation, overview. Binding structure analysis, overview
-
additional information
design and synthesis of 4-anilino-5-carboxamido-2-pyridone MEK1 inhibitors using a combination of medicinal chemistry, computational chemistry, and structural elucidation, overview. Binding structure analysis, overview
-
additional information
design and synthesis of 4-anilino-5-carboxamido-2-pyridone MEK1 inhibitors using a combination of medicinal chemistry, computational chemistry, and structural elucidation, overview. Binding structure analysis, overview
-
additional information
no MEK inhibition by theobromine
-
additional information
-
no MEK inhibition by theobromine
-
additional information
no inhibition of MEK2 by MEK1/ERK1/2-specific inhibitor PD98059
-
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0.01
1-(2,3-dihydroxypropyl)-4-(2-fluoro-4-iodoanilino)-6-oxo-1,6-dihydro-3-pyridinecarboxamide
Mus musculus
above, cascade IC50
0.00489 - 0.0049
1-(3-cyanopropyl)-4-(2-fluoro-4-iodoanilino)-6-oxo-1,6-dihydro-3-pyridinecarboxamide
0.000091 - 0.01
1-allyl-4-(2-fluoro-4-iodoanilino)-6-oxo-1,6-dihydro-3-pyridinecarboxamide
0.001
1-ethyl-4-(2-fluoro-4-iodoanilino)-6-oxo-1,6-dihydro-3-pyridinecarboxamide
0.003
1-methyl-4-(2-naphthylamino)-6-oxo-1,6-dihydro-3-pyridinecarboxamide
0.0000174
3,4-difluoro-2-[(2-fluoro-4-iodophenyl)amino]benzamide
Mus musculus
cascade IC50
0.00254 - 0.005
4-(2-fluoro-4-iodoanilino)-1-(2-hydroxyethyl)-6-oxo-1,6-dihydro-3-pyridinecarboxamide
0.003
4-(2-fluoro-4-iodoanilino)-1-(3-hydroxypropyl)-6-oxo-1,6-dihydro-3-pyridinecarboxamide
0.000004 - 0.000023
4-(2-fluoro-4-iodoanilino)-1-methyl-6-oxo-1,6-dihydro-3-pyridinecarboxamide
0.000425 - 0.005
4-(2-fluoro-4-iodoanilino)-1-methyl-6-oxo-1,6-dihydro-3-pyridinecarboxylic acid
0.00113
4-(2-fluoro-4-iodoanilino)-1-[2-(2-methoxyethoxy)ethyl]-6-oxo-1,6-dihydro-3-pyridinecarboxamide
0.0001 - 0.00063
4-(2-fluoro-4-iodoanilino)-6-oxo-1,6-dihydro-3-pyridinecarboxamide
0.00043 - 0.00254
4-(2-fluoro-4-iodoanilino)-6-oxo-1-propyl-1,6-dihydro-3-pyridinecarboxamide
0.000195
4-(2-fluoro-4-iodoanilino)-N,1-dimethyl-6-oxo-1,6-dihydro-3-pyridinecarboxamide
0.000627 - 1.2
4-(2-fluoro-4-iodoanilino)-N,N,1-trimethyl-6-oxo-1,6-dihydro-3-pyridinecarboxamide
0.000005 - 0.000018
4-(2-fluoro-4-iodoanilino)-N-(2-hydroxyethoxy)-1-methyl-6-oxo-1,6-dihydro-3-pyridinecarboxamide
0.00018 - 0.00021
4-(2-fluoro-4-iodoanilino)-N-(2-hydroxyethyl)-1-methyl-6-oxo-1,6-dihydro-3-pyridinecarboxamide
0.000061 - 0.000095
4-(2-fluoro-4-iodoanilino)-N-(3-hydroxypropyl)-1-methyl-6-oxo-1,6-dihydro-3-pyridinecarboxamide
0.00297
4-(2-fluoro-4-methylanilino)-1-methyl-6-oxo-1,6-dihydro-3-pyridinecarboxamide
0.00015 - 0.00036
4-(2-fluoro-4-methylsulfanylphenylamino)-1-methyl-6-oxo-1,6-dihydro-3 -pyridinecarboxamide
0.0039 - 0.00572
4-(3,4-dichlorophenylamino)-1-methyl-6-oxo-1,6-dihydro-3-pyridinecarboxamide
0.000093 - 0.00191
4-(4-bromo-2-fluoroanilino)-1-methyl-6-oxo-1,6-dihydro-3-pyridinecarboxamide
0.00012 - 0.00363
4-(4-bromo-2-fluoroanilino)-N-(2-hydroxyethoxy)-1-methyl-6-oxo-1,6-dihydro-3-pyridinecarboxamide
0.0000068 - 0.000124
4-(4-bromo-2-fluorophenylamino)-1-methylpyridin-2(1H)-one
Homo sapiens
-
selective anthranilic acid type inhibitors, residues K97, I141, M143, F129, V127, I126, L118, F209, V211, and S212 of MEK1/2 are important for interaction with the inhibitor, noncompetitive to ATP, inhibition of ERK phosphorylation by MEK1/2 by the deriva
0.01
4-(4-cyano-2-fluoroanilino)-1-methyl-6-oxo-1,6-dihydro-3-pyridinecarboxamide
0.00011 - 0.00262
4-(4-ethyl-2-fluoroanilino)-1-methyl-6-oxo-1,6-dihydro-3-pyridinecarboxamide
0.000021 - 0.0001
4-(4-ethynyl-2-fluoroanilino)-1-methyl-6-oxo-1,6-dihydro-3-pyridinecarboxamide
0.0000842
4-amino-1-[3,4-difluoro-2-[(2-fluoro-4-iodophenyl)amino]phenyl]-2-hydroxybutan-1-one
Mus musculus
cascade IC50
0.01
4-[2-fluoro-4-(1,1,2,2,3,3,4,4,4-nonafluorobutyl)anilino]-1-methyl-6-oxo-1,6 -dihydro-3-pyridinecarboxamide
0.01
4-[2-fluoro-4-(3-hydroxypropyl)anilino]-1-methyl-6-oxo-1,6-dihydro-3-pyridinecarboxamide
0.0000012
4-[3,4-difluoro-2-[(2-fluoro-4-iodophenyl)amino]phenyl]-3-hydroxy-4-oxobutanamide
Mus musculus
cascade IC50
0.000052
AS-703026
Homo sapiens
-
inhibition of MEK1, pH and temperature not specified in the publication
0.000019 - 0.000047
BAY 869766
0.0000052
CH4987655
Homo sapiens
-
inhibition of MEK1, pH and temperature not specified in the publication
0.000016 - 0.000046
CI-1040
0.000063 - 0.00067
ethyl 4-(2-fluoro-4-iodoanilino)-1-methyl-6-oxo-1,6-dihydro-3-pyridinecarboxylate
0.000046
LL-Z1640-2
Homo sapiens
-
inhibition of MEK1, pH and temperature not specified in the publication
0.000014
selumetinib
Homo sapiens
-
inhibition of MEK1 phosphorylation of ERK2, pH and temperature not specified in the publication
0.01
tert-butyl [5-(aminocarbonyl)-4-(2-fluoro-4-iodoanilino)-2-oxo-1(2H)-pyridinyl]acetate
Mus musculus
inhibition of the Raf-MEK-ERK cascade in an isolated enzyme assay
0.01
[5-(aminocarbonyl)-4-(2-fluoro-4-iodoanilino)-2-oxo-1(2H)-pyridinyl]acetic acid
Mus musculus
above, cascade IC50
0.00489
1-(3-cyanopropyl)-4-(2-fluoro-4-iodoanilino)-6-oxo-1,6-dihydro-3-pyridinecarboxamide
Mus musculus
inhibition of the Raf-MEK-ERK cascade in an isolated enzyme assay
0.0049
1-(3-cyanopropyl)-4-(2-fluoro-4-iodoanilino)-6-oxo-1,6-dihydro-3-pyridinecarboxamide
Mus musculus
cascade IC50
0.000091
1-allyl-4-(2-fluoro-4-iodoanilino)-6-oxo-1,6-dihydro-3-pyridinecarboxamide
Mus musculus
inhibition of the Raf-MEK-ERK cascade in an isolated enzyme assay
0.00601
1-allyl-4-(2-fluoro-4-iodoanilino)-6-oxo-1,6-dihydro-3-pyridinecarboxamide
Mus musculus
cascade IC50
0.01
1-allyl-4-(2-fluoro-4-iodoanilino)-6-oxo-1,6-dihydro-3-pyridinecarboxamide
Mus musculus
inhibition of the Raf-MEK-ERK cascade in an isolated enzyme assay
0.001
1-ethyl-4-(2-fluoro-4-iodoanilino)-6-oxo-1,6-dihydro-3-pyridinecarboxamide
Mus musculus
inhibition of the Raf-MEK-ERK cascade in an isolated enzyme assay
0.001
1-ethyl-4-(2-fluoro-4-iodoanilino)-6-oxo-1,6-dihydro-3-pyridinecarboxamide
Mus musculus
cascade IC50
0.003
1-methyl-4-(2-naphthylamino)-6-oxo-1,6-dihydro-3-pyridinecarboxamide
Mus musculus
inhibition of the Raf-MEK-ERK cascade in an isolated enzyme assay
0.003
1-methyl-4-(2-naphthylamino)-6-oxo-1,6-dihydro-3-pyridinecarboxamide
Mus musculus
cascade IC50
0.00254
4-(2-fluoro-4-iodoanilino)-1-(2-hydroxyethyl)-6-oxo-1,6-dihydro-3-pyridinecarboxamide
Mus musculus
inhibition of the Raf-MEK-ERK cascade in an isolated enzyme assay
0.005
4-(2-fluoro-4-iodoanilino)-1-(2-hydroxyethyl)-6-oxo-1,6-dihydro-3-pyridinecarboxamide
Mus musculus
colon26 cellular assay
0.005
4-(2-fluoro-4-iodoanilino)-1-(2-hydroxyethyl)-6-oxo-1,6-dihydro-3-pyridinecarboxamide
Mus musculus
above cascade IC50
0.003
4-(2-fluoro-4-iodoanilino)-1-(3-hydroxypropyl)-6-oxo-1,6-dihydro-3-pyridinecarboxamide
Mus musculus
inhibition of the Raf-MEK-ERK cascade in an isolated enzyme assay
0.003
4-(2-fluoro-4-iodoanilino)-1-(3-hydroxypropyl)-6-oxo-1,6-dihydro-3-pyridinecarboxamide
Mus musculus
above, cascade IC50
0.000004
4-(2-fluoro-4-iodoanilino)-1-methyl-6-oxo-1,6-dihydro-3-pyridinecarboxamide
Mus musculus
colon26 cellular assay
0.000023
4-(2-fluoro-4-iodoanilino)-1-methyl-6-oxo-1,6-dihydro-3-pyridinecarboxamide
Mus musculus
inhibition of the Raf-MEK-ERK cascade in an isolated enzyme assay
0.000023
4-(2-fluoro-4-iodoanilino)-1-methyl-6-oxo-1,6-dihydro-3-pyridinecarboxamide
Mus musculus
cascade IC50
0.000425
4-(2-fluoro-4-iodoanilino)-1-methyl-6-oxo-1,6-dihydro-3-pyridinecarboxylic acid
Mus musculus
inhibition of the Raf-MEK-ERK cascade in an isolated enzyme assay
0.000425
4-(2-fluoro-4-iodoanilino)-1-methyl-6-oxo-1,6-dihydro-3-pyridinecarboxylic acid
Mus musculus
cascade IC50
0.005
4-(2-fluoro-4-iodoanilino)-1-methyl-6-oxo-1,6-dihydro-3-pyridinecarboxylic acid
Mus musculus
colon26 cellular assay
0.00113
4-(2-fluoro-4-iodoanilino)-1-[2-(2-methoxyethoxy)ethyl]-6-oxo-1,6-dihydro-3-pyridinecarboxamide
Mus musculus
inhibition of the Raf-MEK-ERK cascade in an isolated enzyme assay
0.00113
4-(2-fluoro-4-iodoanilino)-1-[2-(2-methoxyethoxy)ethyl]-6-oxo-1,6-dihydro-3-pyridinecarboxamide
Mus musculus
cascade IC50
0.0001
4-(2-fluoro-4-iodoanilino)-6-oxo-1,6-dihydro-3-pyridinecarboxamide
Mus musculus
inhibition of the Raf-MEK-ERK cascade in an isolated enzyme assay
0.0001
4-(2-fluoro-4-iodoanilino)-6-oxo-1,6-dihydro-3-pyridinecarboxamide
Mus musculus
cascade IC50
0.00063
4-(2-fluoro-4-iodoanilino)-6-oxo-1,6-dihydro-3-pyridinecarboxamide
Mus musculus
colon26 cellular assay
0.00043
4-(2-fluoro-4-iodoanilino)-6-oxo-1-propyl-1,6-dihydro-3-pyridinecarboxamide
Mus musculus
colon26 cellular assay
0.00254
4-(2-fluoro-4-iodoanilino)-6-oxo-1-propyl-1,6-dihydro-3-pyridinecarboxamide
Mus musculus
inhibition of the Raf-MEK-ERK cascade in an isolated enzyme assay
0.00254
4-(2-fluoro-4-iodoanilino)-6-oxo-1-propyl-1,6-dihydro-3-pyridinecarboxamide
Mus musculus
cascade IC50
0.000195
4-(2-fluoro-4-iodoanilino)-N,1-dimethyl-6-oxo-1,6-dihydro-3-pyridinecarboxamide
Mus musculus
inhibition of the Raf-MEK-ERK cascade in an isolated enzyme assay
0.000195
4-(2-fluoro-4-iodoanilino)-N,1-dimethyl-6-oxo-1,6-dihydro-3-pyridinecarboxamide
Mus musculus
cascade IC50
0.000627
4-(2-fluoro-4-iodoanilino)-N,N,1-trimethyl-6-oxo-1,6-dihydro-3-pyridinecarboxamide
Mus musculus
inhibition of the Raf-MEK-ERK cascade in an isolated enzyme assay
1.2
4-(2-fluoro-4-iodoanilino)-N,N,1-trimethyl-6-oxo-1,6-dihydro-3-pyridinecarboxamide
Mus musculus
cascade IC50
0.000005
4-(2-fluoro-4-iodoanilino)-N-(2-hydroxyethoxy)-1-methyl-6-oxo-1,6-dihydro-3-pyridinecarboxamide
Mus musculus
colon26 cellular assay
0.000018
4-(2-fluoro-4-iodoanilino)-N-(2-hydroxyethoxy)-1-methyl-6-oxo-1,6-dihydro-3-pyridinecarboxamide
Mus musculus
inhibition of the Raf-MEK-ERK cascade in an isolated enzyme assay
0.000018
4-(2-fluoro-4-iodoanilino)-N-(2-hydroxyethoxy)-1-methyl-6-oxo-1,6-dihydro-3-pyridinecarboxamide
Mus musculus
cascade IC50
0.00018
4-(2-fluoro-4-iodoanilino)-N-(2-hydroxyethyl)-1-methyl-6-oxo-1,6-dihydro-3-pyridinecarboxamide
Mus musculus
colon26 cellular assay
0.000206
4-(2-fluoro-4-iodoanilino)-N-(2-hydroxyethyl)-1-methyl-6-oxo-1,6-dihydro-3-pyridinecarboxamide
Mus musculus
inhibition of the Raf-MEK-ERK cascade in an isolated enzyme assay
0.00021
4-(2-fluoro-4-iodoanilino)-N-(2-hydroxyethyl)-1-methyl-6-oxo-1,6-dihydro-3-pyridinecarboxamide
Mus musculus
cascade IC50
0.000061
4-(2-fluoro-4-iodoanilino)-N-(3-hydroxypropyl)-1-methyl-6-oxo-1,6-dihydro-3-pyridinecarboxamide
Mus musculus
inhibition of the Raf-MEK-ERK cascade in an isolated enzyme assay
0.000061
4-(2-fluoro-4-iodoanilino)-N-(3-hydroxypropyl)-1-methyl-6-oxo-1,6-dihydro-3-pyridinecarboxamide
Mus musculus
cascade IC50
0.000095
4-(2-fluoro-4-iodoanilino)-N-(3-hydroxypropyl)-1-methyl-6-oxo-1,6-dihydro-3-pyridinecarboxamide
Mus musculus
colon26 cellular assayy
0.00297
4-(2-fluoro-4-methylanilino)-1-methyl-6-oxo-1,6-dihydro-3-pyridinecarboxamide
Mus musculus
inhibition of the Raf-MEK-ERK cascade in an isolated enzyme assay
0.00297
4-(2-fluoro-4-methylanilino)-1-methyl-6-oxo-1,6-dihydro-3-pyridinecarboxamide
Mus musculus
cascade IC50
0.00015
4-(2-fluoro-4-methylsulfanylphenylamino)-1-methyl-6-oxo-1,6-dihydro-3 -pyridinecarboxamide
Mus musculus
colon26 cellular assay
0.000356
4-(2-fluoro-4-methylsulfanylphenylamino)-1-methyl-6-oxo-1,6-dihydro-3 -pyridinecarboxamide
Mus musculus
inhibition of the Raf-MEK-ERK cascade in an isolated enzyme assay
0.00036
4-(2-fluoro-4-methylsulfanylphenylamino)-1-methyl-6-oxo-1,6-dihydro-3 -pyridinecarboxamide
Mus musculus
cascade IC50
0.0039
4-(3,4-dichlorophenylamino)-1-methyl-6-oxo-1,6-dihydro-3-pyridinecarboxamide
Mus musculus
colon26 cellular assay
0.0057
4-(3,4-dichlorophenylamino)-1-methyl-6-oxo-1,6-dihydro-3-pyridinecarboxamide
Mus musculus
cascade IC50
0.00572
4-(3,4-dichlorophenylamino)-1-methyl-6-oxo-1,6-dihydro-3-pyridinecarboxamide
Mus musculus
inhibition of the Raf-MEK-ERK cascade in an isolated enzyme assay
0.000093
4-(4-bromo-2-fluoroanilino)-1-methyl-6-oxo-1,6-dihydro-3-pyridinecarboxamide
Mus musculus
colon26 cellular assay
0.0019
4-(4-bromo-2-fluoroanilino)-1-methyl-6-oxo-1,6-dihydro-3-pyridinecarboxamide
Mus musculus
cascade IC50
0.00191
4-(4-bromo-2-fluoroanilino)-1-methyl-6-oxo-1,6-dihydro-3-pyridinecarboxamide
Mus musculus
inhibition of the Raf-MEK-ERK cascade in an isolated enzyme assay
0.00012
4-(4-bromo-2-fluoroanilino)-N-(2-hydroxyethoxy)-1-methyl-6-oxo-1,6-dihydro-3-pyridinecarboxamide
Mus musculus
colon26 cellular assay
0.00363
4-(4-bromo-2-fluoroanilino)-N-(2-hydroxyethoxy)-1-methyl-6-oxo-1,6-dihydro-3-pyridinecarboxamide
Mus musculus
inhibition of the Raf-MEK-ERK cascade in an isolated enzyme assay
0.00363
4-(4-bromo-2-fluoroanilino)-N-(2-hydroxyethoxy)-1-methyl-6-oxo-1,6-dihydro-3-pyridinecarboxamide
Mus musculus
cascade IC50
0.01
4-(4-cyano-2-fluoroanilino)-1-methyl-6-oxo-1,6-dihydro-3-pyridinecarboxamide
Mus musculus
inhibition of the Raf-MEK-ERK cascade in an isolated enzyme assay
0.01
4-(4-cyano-2-fluoroanilino)-1-methyl-6-oxo-1,6-dihydro-3-pyridinecarboxamide
Mus musculus
above, cascade IC50
0.00011
4-(4-ethyl-2-fluoroanilino)-1-methyl-6-oxo-1,6-dihydro-3-pyridinecarboxamide
Mus musculus
colon26 cellular assay
0.00262
4-(4-ethyl-2-fluoroanilino)-1-methyl-6-oxo-1,6-dihydro-3-pyridinecarboxamide
Mus musculus
inhibition of the Raf-MEK-ERK cascade in an isolated enzyme assay
0.00262
4-(4-ethyl-2-fluoroanilino)-1-methyl-6-oxo-1,6-dihydro-3-pyridinecarboxamide
Mus musculus
cascade IC50
0.000021
4-(4-ethynyl-2-fluoroanilino)-1-methyl-6-oxo-1,6-dihydro-3-pyridinecarboxamide
Mus musculus
colon26 cellular assay
0.0001
4-(4-ethynyl-2-fluoroanilino)-1-methyl-6-oxo-1,6-dihydro-3-pyridinecarboxamide
Mus musculus
inhibition of the Raf-MEK-ERK cascade in an isolated enzyme assay
0.0001
4-(4-ethynyl-2-fluoroanilino)-1-methyl-6-oxo-1,6-dihydro-3-pyridinecarboxamide
Mus musculus
cascade IC50
0.01
4-[2-fluoro-4-(1,1,2,2,3,3,4,4,4-nonafluorobutyl)anilino]-1-methyl-6-oxo-1,6 -dihydro-3-pyridinecarboxamide
Mus musculus
inhibition of the Raf-MEK-ERK cascade in an isolated enzyme assay
0.01
4-[2-fluoro-4-(1,1,2,2,3,3,4,4,4-nonafluorobutyl)anilino]-1-methyl-6-oxo-1,6 -dihydro-3-pyridinecarboxamide
Mus musculus
above, cascade IC50
0.01
4-[2-fluoro-4-(3-hydroxypropyl)anilino]-1-methyl-6-oxo-1,6-dihydro-3-pyridinecarboxamide
Mus musculus
inhibition of the Raf-MEK-ERK cascade in an isolated enzyme assay
0.01
4-[2-fluoro-4-(3-hydroxypropyl)anilino]-1-methyl-6-oxo-1,6-dihydro-3-pyridinecarboxamide
Mus musculus
above, cascade IC50
0.000019
BAY 869766
Homo sapiens
-
inhibition of MEK1, pH and temperature not specified in the publication
0.000047
BAY 869766
Homo sapiens
-
inhibition of MEK2, pH and temperature not specified in the publication
0.000016
CI-1040
Mus musculus
clinical candidate, inhibition of the Raf-MEK-ERK cascade in an isolated enzyme assay
0.000046
CI-1040
Mus musculus
clinical candidate, colon26 cellular assay
0.000063
ethyl 4-(2-fluoro-4-iodoanilino)-1-methyl-6-oxo-1,6-dihydro-3-pyridinecarboxylate
Mus musculus
colon26 cellular assay
0.000669
ethyl 4-(2-fluoro-4-iodoanilino)-1-methyl-6-oxo-1,6-dihydro-3-pyridinecarboxylate
Mus musculus
inhibition of the Raf-MEK-ERK cascade in an isolated enzyme assay
0.00067
ethyl 4-(2-fluoro-4-iodoanilino)-1-methyl-6-oxo-1,6-dihydro-3-pyridinecarboxylate
Mus musculus
cascade IC50
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evolution
bos5 from Botrytis cinerea, a gene that encodes a mitogen-activated protein kinase kinase (MAPKK), is homologous to OS-5 of Neurospora crassa
evolution
the enzyme is a member of the MAP kinase family
evolution
the protozoan pathogen, Trypanosoma brucei brucei, possesses many protein kinases which show high homology to the catalytic domains of mitogen activated protein kinases (MAPKs) and their upstream regulators. The close relationship of MKK and MKKK kinase domains combined with the phylogenetic distance between trypanosomatids and model organisms makes direct experimentation required to delineate functional attributes of the parasite kinases
evolution
-
bos5 from Botrytis cinerea, a gene that encodes a mitogen-activated protein kinase kinase (MAPKK), is homologous to OS-5 of Neurospora crassa
-
evolution
-
the protozoan pathogen, Trypanosoma brucei brucei, possesses many protein kinases which show high homology to the catalytic domains of mitogen activated protein kinases (MAPKs) and their upstream regulators. The close relationship of MKK and MKKK kinase domains combined with the phylogenetic distance between trypanosomatids and model organisms makes direct experimentation required to delineate functional attributes of the parasite kinases
-
malfunction
an mkk3 mutant shows both a hypersensitive response in plant hormone gibberellin and a less sensitive response in red light signaling. Light-induced MAPK activation in wild-type seedlings and constitutive MAPK phosphorylation in dark-grown mkk3 mutant seedlings are found, respectively. The mkk3-1 mutant displays a gibberellic acid-hypersensitive phenotype in hypocotyl elongation, with an additiona long petiole phenotype
malfunction
bloodstream forms lacking MKK1 show decreased growth at 39°C as compared to the parental line, enzyme knockout phenotype, overview. The two mkk1 knockout clones are moderately more sensitive to temperature stress than the wild-type
malfunction
-
D-domain mutant CAMKK7DELTAD is inactive toward MPK6 but the activity toward MPK3 is maintained, and the CAMKK7DELTAD mutant loses stomatal cluster-promoting activity
malfunction
enzyme knockout phenotype, overview
malfunction
enzyme mutants show embryonic lethality. Mkk4 knockout embryonic stem cells exhibit diminished p-ATF2 and MEF2C expression, resulting in impaired MHC induction and defective cardiomyocyte differdifferentiation. Loss of MKK4 significantly blocks the induction of Mhca and Mhcb, but had no effect on expression of Mlc. Exogenous MKK4 expression partially restores the ability of Mkk4-/- embryonic stem cells to differentiate into cardiomyocytes. Mice lacking either MKK4 or MKK7 display an analogous embryonic lethal phenotype that may be attributed, at least in part, to insufficient JNK activation
malfunction
enzyme mutants show embryonic lethality. Mkk7 knockout embryonic stem cells show elevated phosphorylation of MKK4, p38, and ATF2, and increased MEF2C expression. The mutant cells show higher expression of MHC and MLC and enhanced formation of contractile cardiomyocytes. Mice lacking either MKK4 or MKK7 display an analogous embryonic lethal phenotype that may be attributed, at least in part, to insufficient JNK activation
malfunction
enzyme ZmMKK1 overexpression in Arabidopsis thaliana plants enhances the tolerance to salt and drought stresses, and the expression of ROS scavenging enzyme- and ABA-related genes, such as POD, CAT, RAB18 and RD29A under salt and drought conditions. ZmMKK1-overexpressing Arabidopsis plants show enhanced sensitivity to abscisic acid in seed germination, root length and stomata aperture
malfunction
expression of iron superoxide dismutases FSD2 and FSD3 is significantly increased in Arabidopsis in response to NaCl treatment but blocked in transgenic MKK5-RNAi plant, mkk5. Overexpression of MKK5 in wild-type plants enhances their tolerance to salt treatments, while the mkk5 mutant exhibits hypersensitivity to salt stress in germination on salt-containing media. The kinase activity of MPK6 is totally turned off in mkk5, whereas the activity of MPK3 is only partially blocked. MKK5-overexpressing plants exhibit salt tolerance phenotypes
malfunction
genetic inactivation of MKK7 results in an extended period of oscillation in circadian gene expression in mouse embryonic fibroblasts, genetic inactivation of the Mkk7 gene alters circadian gene expression
malfunction
genetic inactivation of the Mkk7 gene alters circadian gene expression
malfunction
-
in both CAMKK4 and CAMKK5, removal of the entire N terminus (CAMKK4/5DELTANextDNint) renders the kinases incapable of inhibiting development during the SPCH and MUTE stages. As with CAMKK4/5 variants lacking D-domains, CAMKK7/9DD variants are generally unable to inhibit stomatal development in the SPCH and MUTE stages
malfunction
knockdown expression of SIP2 via RNA interference (RNAi) results in drastic reduction of nodules formed in transgenic hairy roots. In these roots, the expression levels of SIP2 and three marker genes for infection thread and nodule primordium formation are downregulated drastically, while the expression of two other MAPKK genes are not altered
malfunction
MKK4 is highly mutated and has a pro-oncogenic role in cancers of pancreatic, breast, colon, prostate, skin, and laryngeal squamous cell. Strong association between -1304T>G (rs3826392) polymorphism in the promoter of MKK4 gene and a decreased risk of sporadic colorectal cancer in a southern Chinese population, overview
malfunction
overexpression of MEK2 significantly promotes the replication of classical swine fever virus,CSFV, whereas knockdown of MEK2 by lentivirus-mediated small hairpin RNAs dramatically inhibits CSFV replication
malfunction
small grain 1, smg1, mutants exhibit small and light grains, dense and erect panicles and comparatively slightly shorter plants. The short grain and panicle phenotypes of smg1 mutants are caused by a defect in cell proliferation. Mutant smg1 forms dense and erect panicles. Mutant phenotype, overview
malfunction
the bos5 gene deletion mutant exhibits reduced vegetative growth and strongly impaired conidiation. The mutant also exhibits increased sensitivity to the dicarboximide fungicide iprodione and to osmotic stress mediated by NaCl or KCl. The BcSAK1 protein, the putative downstream component of BOS5, is not phosphorylated in the mutant. Plant inoculation tests show that the mutants are unable to infect cucumber leaves. All of these defects are restored by genetic complementation of the DELTAbcos5-21 mutant with the wild-type bos5 gene
malfunction
-
VdPbs2 deletion strains exhibit delayed melanin synthesis and reduced formation of microsclerotia, similar to a VdHog1 deletion mutant. When exposed to stresses, VdPbs2 mutants are more sensitive than the wild-type to osmotic agents and peroxide, but more resistant to inhibitors of cell wall synthesis and some fungicides. VdPbs2 deletion mutants exhibit reduced virulence on smoke tree and tobacco seedlings. Transcript analysis revealed´s that three genes(VDAG_08724, VDAG_03661,and VDAG_06340) are consistently downregulated in the 1VdPbs2 mutant compared to that of the wild-type after treated with 1 mM H2O2 for 30 min. Phentypes, overview
malfunction
virulence on chestnut and the developmental steps essential for mating are not affected in the DELTAcpkk3 strain. No alterations are reported in DELTAcpkk3, except under hyperosmotic conditions and in the presence of fludioxonil. Phenotype, overview
malfunction
virulence on chestnut is affected in the DELTAcpkk1 strain which is also unable to complete the developmental steps essential for mating. Phenotype, overview
malfunction
virulence on chestnut is affected in the DELTAcpkk2 strain which is also unable to complete the developmental steps essential for mating. DELTAcpkk2 mutants show higher sensitivity during growth in medium containing the antibiotic G418, i.e. geneticin. Phenotype, overview
malfunction
-
VdPbs2 deletion strains exhibit delayed melanin synthesis and reduced formation of microsclerotia, similar to a VdHog1 deletion mutant. When exposed to stresses, VdPbs2 mutants are more sensitive than the wild-type to osmotic agents and peroxide, but more resistant to inhibitors of cell wall synthesis and some fungicides. VdPbs2 deletion mutants exhibit reduced virulence on smoke tree and tobacco seedlings. Transcript analysis revealed´s that three genes(VDAG_08724, VDAG_03661,and VDAG_06340) are consistently downregulated in the 1VdPbs2 mutant compared to that of the wild-type after treated with 1 mM H2O2 for 30 min. Phentypes, overview
-
malfunction
-
the bos5 gene deletion mutant exhibits reduced vegetative growth and strongly impaired conidiation. The mutant also exhibits increased sensitivity to the dicarboximide fungicide iprodione and to osmotic stress mediated by NaCl or KCl. The BcSAK1 protein, the putative downstream component of BOS5, is not phosphorylated in the mutant. Plant inoculation tests show that the mutants are unable to infect cucumber leaves. All of these defects are restored by genetic complementation of the DELTAbcos5-21 mutant with the wild-type bos5 gene
-
malfunction
-
enzyme knockout phenotype, overview
-
malfunction
-
bloodstream forms lacking MKK1 show decreased growth at 39°C as compared to the parental line, enzyme knockout phenotype, overview. The two mkk1 knockout clones are moderately more sensitive to temperature stress than the wild-type
-
metabolism
Cpkk1, the Mkk1 orthologue, acts in a phosphorylation cascade essential for cell integrity
metabolism
Cpkk2 is the Ste7 orthologue involved in the pheromone response pathway
metabolism
Cpkk3 is the Pbs2 orthologue, the MAP2K activates during the high-osmolarity response
metabolism
-
MAPK forms the backbone of four primary signal transduction cascades leading to the phosphorylation and activation of extracellular signal-regulated kinases 1 and 2 (ERK1-2), JNK, p38 and ERK5. The RAS-RAF-MEK-ERK pathway acts as a conduit to transduce signals from receptor tyrosine kinases (RTKs) to the nucleus. This pathway is intimately tied to intracellular machinery involved in cell proliferation, survival and cell migration, overview
metabolism
MEK1 activates the prototypic MAPK pathway by activating enzyme ERK1
metabolism
mitogen-activated protein kinase (MAPK) cascades play critical roles in signal transduction processes in eukaryotes. The MAPK kinases (MAPKKs) that link MAPKK kinases (MAPKKKs) and MAPKs are key components of MAPK cascades
metabolism
mitogen-activated protein kinase kinase 2 (MEK2) is a kinase that operates immediately upstream of extracellular regulated kinase 1/2 (ERK1/2) and links to Raf and ERK via phosphorylation. The mitogen-activated protein kinase kinase/extracellular regulated kinase (MEK1/2/ERK1/2) cascade is involved in the replication of several members of the Flaviviridae family, including hepatitis C virus and dengue virus, or of classical swine fever virus, a psetivirus in swine
metabolism
MKK4 belongs to MAPK pathways known to have involvement in the regulation of apoptosis, inflammation, and tumorigenesis
metabolism
signal transduction pathways are integral components of the developmental regulatory network that guides progressive cell fate determination. Essential enzymes MKK4 and MKK7 are upstream kinases of the mitogen-activated protein kinases (MAPKs), responsible for channeling physiological and environmental signals to their cellular responses. In vitro, MKK4 and MKK7 are dispensable for in embryonic stem cell self-renewal and pluripotency maintenance, but they exhibit unique signaling and functional properties in differentiation. MKK4 and MKK7 complemented each other in activation of the JNK-c-Jun cascades and loss of both leads to senescence upon cell differentiation.On the other hand, MKK4 and MKK7 have opposite effects on activation of the p38 cascades during differentiation, MKK4 is required for cardiomyocyte differentiation, while MKK7 represses it
metabolism
te enzyme MKK5 is part of the MAP kinase cascade, including MEKK1, MKK5, and MPK6, that mediates the salt-induced expression of iron superoxide dismutases. MKK5 interactes with the MEKK1 protein that is also involved in the salt-induced FSD signalling pathway. Salt-induced iron superoxide dismutases FSD2 and FSD3 expressions are influenced by MEKK1 via MKK5-MPK6-coupled signalling. MPK6 is also involved in the MKK5-mediated iron superoxide dismutase signalling pathway in salt stress. The MKK5-MPK3/MPK6 pathway is similar to the flagellin-induced MAPK signalling pathway, MKK4/MKK5-MPK3/MPK6
metabolism
the enzyme is involved in the MAPK signalling network in Oryza sativa
metabolism
the mitogen activated protein kinase (MAPK) kinase (MKK) is a key component of MAPK cascade that plays important roles in intra and extra cellular signaling in plants
metabolism
the mitogen activated protein kinase kinase (MAPKK) is the central module of MAPK cascade and also a point of signal integration and divergence
metabolism
the mitogen-activated protein kinase (MAPK) cascade usually functions as an important signaling network involved in physiological and developmental processes in eukaryotes. The MAPK cascade is usually composed of sequential activations of three classes of Ser/Thr protein kinases: MAPK (MPK), MAPK kinase (MKK), and MAPK kinase kinase (MKKK). The MAPK kinase (MKK) gene family has relatively few members in canonical MAPK cascade gene families, which are classified into four groups (A to D) based on the sequence similarities
metabolism
the p38 pathway is activated by MKK3, MKK4, and MKK6
physiological function
enzyme ZmMKK1 might act as an ABA- and ROS-dependent protein kinase in positive modulation of salt and drought tolerance. ZmMKK1 prevents chlorophylls degradation to maintain plants photosynthesis under salt stress, and ZmMKK1 enhances the drought tolerance of transgenic plants
physiological function
gene SMG1 encodes enzyme MKK4 (OsMKK4), which influences grain size by promoting cell proliferation, SMG1 influences panicle size and shape. OsMKK4 influences brassinosteroid (BR) responses and the expression of BR-related genes. Enzyme OsMKK4 is a factor for grain size, and links the MAPK pathways and brassinosteroids in grain growth
physiological function
GhMKK3 plays an important role in drought tolerance in cotton. Expression of GhPIP1 and GhMPK7 is induced in a MKK3-dependent manner by abscisic acid and drought
physiological function
identification and analysis of the interaction network between members of Oryza sativa mitogen activated protein kinase kinase (MAPKK) and mitogen activated protein kinase (MAPK) overview
physiological function
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isozymes MKK4/5/7/9 affect stomatal development, the D-domains of MKK7/9 are important in regulating subcellular localization of the kinases and this localization is necessary for stomatal promoting activity, overview. Additional regions of MKK4/5 function as MKK specificity determinants in vivo. A 14-3-3 binding site in the D-domain of MKK4 contributes to MKK4 function. When rendered constitutively active, four MAPK kinases (MKKs), MKK4/5/7/9, are capable of perturbing stomatal development, the kinases comprise two pairs, MKK4/5 and MKK7/9, with both overlapping and divergent functions. The behavior of MKK4 mirrors that of MKK5 and MKK7 mirrors that of MKK9 in the stomatal lineage
physiological function
-
isozymes MKK4/5/7/9 affect stomatal development, the D-domains of MKK7/9 are important in regulating subcellular localization of the kinases and this localization is necessary for stomatal promoting activity, overview. Additional regions of MKK4/5 function as MKK specificity determinants in vivo. When rendered constitutively active, four MAPK kinases (MKKs), MKK4/5/7/9, are capable of perturbing stomatal development, the kinases comprise two pairs, MKK4/5 and MKK7/9, with both overlapping and divergent functions. The behavior of MKK4 mirrors that of MKK5 and MKK7 mirrors that of MKK9 in the stomatal lineage
physiological function
-
isozymes MKK4/5/7/9 affect stomatal development, the D-domains of MKK7/9 are important in regulating subcellular localization of the kinases and this localization is necessary for stomatal promoting activity, overview. When rendered constitutively active, four MAPK kinases (MKKs), MKK4/5/7/9, are capable of perturbing stomatal development, the kinases comprise two pairs, MKK4/5 and MKK7/9, with both overlapping and divergent functions. The behavior of MKK4 mirrors that of MKK5 and MKK7 mirrors that of MKK9 in the stomatal lineage
physiological function
-
MEK signaling directly impacts both the expression of these cytokines and their downstream activation pathways
physiological function
mitogen activated kinase kinase gene MKK1 is not essential in the pathogenic bloodstream stage of Trypanosoma brucei, no effcts on growth and virulence either in vitro or in vivo. Trypanosoma brucei MKK1 does not appear to play a significant role in flagellar biogenesis
physiological function
mitogen activated kinase kinase gene MKK5 is not essential in the pathogenic bloodstream stage of Trypanosoma brucei, no effcts on growth and virulence either in vitro or in vivo
physiological function
mitogen-activated protein kinase kinase 2, a novel E2-interacting protein, promotes the growth of classical swine fever virus, CSFV, via attenuation of the JAK-STAT signaling pathway. The MEK2-E2 interaction occurs during the late stage of CSFV replication and requires the C-termini of MEK2, residues 266 to 400, and E2
physiological function
mitogen-activated protein kinase kinase 3, MKK3, overexpression induces cell cycle arrest via p38 activation mediated Bmi-1 downregulation in hepatocellular carcinoma. MKK3 as a tumor suppressor. MKK3 overexpression suppresses HepG2 and PLC-PRF-5 cell proliferation and induces cell cycle arrest in the two cell lines. In addition, MKK3 overexpression upregulates the cyclin-dependent kinase inhibitors, p16 INK4A and p15 INK4B in hepatocellular carcinoma cells. Their negative regulator, Bim?1, is downregulated following MKK3 overexpression. MKK3 activates p38 in hepatocellular carcinoma cells and SB203580, a p38 inhibitor, reverses the tumor suppressive effect of MKK3
physiological function
mitogen-activated protein kinase kinase 4 (MAP2K4) plays a crucial role in the stress-activated signal cascade and is enzymatically regulated by ligand or substrate binding, and/or post-translational modification
physiological function
-
mitogen-activated protein kinase kinase VdPbs2 is a key regulator of microsclerotia formation, oxidative stress and fungicide response and plant virulence in Verticillium dahliae via regulating the activity of VdHog1, a mitogen-activated protein kinase, MAPK. VdPbs2 and VdHog1 function in a cascade that regulates microsclerotia formation and virulence, but not all VdHog1 dependent functions are VdPbs2 regulated. VdPbs2 is essential for the oxidative stress response and is required for plant infection, VdPbs2 may be involved in the penetration process during plant infection
physiological function
MKK3 acts in negative regulation in darkness and in light-induced MAPK activation during darklight transition
physiological function
MKK4 regulates Jun N-terminal kinase (JNK) and differentiating cell survival. And MKK4 is required for p38 activation and cardiomyocyte differentiation. Enzymes MKK4 and MKK7 have complementary and distinct roles in embryonic stem cell differentiation
physiological function
MKK7 regulates Jun N-terminal kinase (JNK) and differentiating cell survival. Enzymes MKK4 and MKK7 have complementary and distinct roles in embryonic stem cell differentiation. MKK7 reduces p38 activation
physiological function
regulatory role of gene OsMKK6 on its regulon of genes, possible physiological role of OsMKK6 in modulating gene expression and signaling pathways during different stresses
physiological function
role of OsMKK6 gene in salt stress signaling in rice. Constitutively active OsMKK6 overexpressing rice plants exhibit higher salt stress tolerance, overview
physiological function
SIP2 represents a typical plant mitogen-activated protein kinase kinase (MAPKK) and exhibits autophosphorylation and transphosphorylation activities. SymRK may serve as a negative regulator of the SIP2 signaling pathway. SymRK and SIP2 interaqct and are both protein kinases. The kinase domain of SIP2 is responsible for its interaction with SymRK. Essential role of SIP2 in the early symbiosis signaling and nodule organogenesis
physiological function
the enzyme plays a key role in multiple physiologic and pathophysiologic processes such as inflammation and tumor suppression
physiological function
the enzyme plays a role in MAPK signalling cascades involved in salt stress responses
physiological function
the mitogen-activated protein kinase kinase BOS5 is involved in regulating vegetative differentiation and virulence in Botrytis cinerea
physiological function
the stress kinase mitogen-activated protein kinase kinase 7 (MKK7) is a specific activator of c-Jun N-terminal kinase (JNK), which controls various physiological processes, such as cell proliferation, apoptosis, differentiation, and migration. Involvement of stress kinase mitogen-activated protein kinase kinase 7 in regulation of mammalian circadian clock, overview. JNK interacts with PER2 at both the exogenous and endogenous levels, and MKK7-mediated JNK activation increases the half-life of PER2 protein by inhibiting its ubiquitination. The PER2 protein stabilization induced by MKK7-JNK fusion protein reduces the degradation of PER2 induced by casein kinase 1epsilon. MKK7 controls circadian gene expression in cultured cells
physiological function
the stress kinase mitogen-activated protein kinase kinase 7 (MKK7) is a specific activator of c-Jun N-terminal kinase (JNK), which controls various physiological processes, such as cell proliferation, apoptosis, differentiation, and migration. Involvement of stress kinase mitogen-activated protein kinase kinase 7 in regulation of mammalian circadian clock, overview. JNK interacts with PER2 at both the exogenous and endogenous levels, and MKK7-mediated JNK activation increases the half-life of PER2 protein by inhibiting its ubiquitination. The PER2 protein stabilization induced by MKK7-JNK fusion protein reduces the degradation of PER2 induced by casein kinase 1epsilon. MKK7 controls circadian gene expression in cultured cells
physiological function
transcriptional activity of MyoD is critical in understanding skeletal muscle development and regeneration. Mitogen-activated protein kinase kinase 1 (MEK1) stabilizes MyoD through direct phosphorylation at tyrosine 156 during myogenic differentiation. The amount of MyoD co-precipitated with MAFbx/AT-1 is reduced in the presence of active MEK1. The phosphorylation probably interrupts the binding of MAFbx/AT-1 to MyoD and thereby increases its stability. The MEK1-induced phosphorylation of MyoD enhances heterodimerization with E proteins
physiological function
-
alternative splicing of MEK1 leads to variants MEK1-X1 and MEK1-X2 both localized in the cytoplasm. MEK1-X2 is induced by salt stress. Overexpression of MEK1-X2 leads to a higher increase rate of glycerol production compared to the control and MEK1-X1 overexpression under salt stress. Under salt stress, the expression of GPDH2/3/5/6 increases in MEK1-X2 overexpression strains compared to the control. Overexpression of MEK1-X1 increases the proline content and reduces the malondialdehyde content under salt stress, and MEK1-X1 is able to regulate oxidative stress. MEK1-X2 can interact with MAPKKK1/2/3/9/10/17 and MAPK1. MEK1-X1 interacts with neither upstream MAPKKK nor downstream MAPK. MEK1-X2 overexpressing transgenic lines increase the expression of MAPKKK1/3/10/17 and MAPK1, and MEK1-X2 RNAi lines decrease the expression of MAPKKK2/10/17
physiological function
disruption of the PBS2 gene leads to sensitivity to hyperosmosis and high salt concentration as well as resistance to the fungicide fludioxonil. No obvious difference in virulence is observed between the null mutant and the wild-type strain
physiological function
expression of active MKK10 induces cell death in both maize mesophyll protoplasts and transgenic Arabidopsis thaliana plants. MKK10 leads to MPK3 and MPK6 activation, ROS accumulation and ethylene production in Arabidopsis thaliana. Maize MPK3 and MPK7, the orthologues of Arabidopsis MPK3 and MPK6, interact and are phosphorylated by MKK10 in vitro. MKK10-induced cell death in Arabidopsis thaliana transgenic plants requires the activation of MPK6 and MPK3, and production of ethylene and ROS is involved in MKK10-induced cell death
physiological function
isoform MKK7gamma, product of alternative splicing, binds directly to calcineurin through its PIIVIT motif in vitro, immunoprecipitates with calcineurin from cell extracts, and exhibits fluorescence resonance energy transfer with calcineurin in the cytoplasm but not in the nucleus of living cells. Isoforms alpha and beta exhibit no direct binding or fluorescence resonance energy transfer with calcineurin and are localized more in the nucleus than the cytoplasm. The inhibition of calcineurin phosphatase activity increases the basal phosphorylation of MKK7gamma but not MKK7beta. Deletion of the MKK7gamma PIIVIT motif eliminates FRET with calcineurin and promotes MKK7gamma redistribution to the nucleus. The inhibition of calcineurin phosphatase activity in vascular smooth muscle cells, which express MKK7gamma mRNA, enhances c-Jun N-terminal kinase activation
physiological function
kinase p38alpha MAPK is activated and forms a disulfide-bound heterodimer with MAP2K3 (MKK3) in rat cardiomyocytes and isolated hearts exposed to H2O2. The disulfide heterodimer is sensitive to reduction by mercaptoethanol and is enhanced by the thioredoxin-reductase inhibitor auranofin. The C119S mutation of p38alpha decreases whereas the C162S mutation increases the dimer formation. Disulfide heterodimer formation is abolished in H9C2 cells expressing both MKK3 and p38alpha C119S/C162S and subjected to simulated ischemia and reperfusion. The p38alphaC119S/C162S mutants do not exhibit appreciable alteration in activating dual phosphorylation
physiological function
mitogen-activated protein kinase kinase MKK9 is involved in plant N responses by regulating production of anthocyanins and the ability of N acquisition under low N conditions. Transgenic plants that express a constitutively active version of MKK9 show decreased accumulation of anthocynanins and reduced expression of key anthocyanin biosynthetic genes under low N condition compared to the plants expressing the inactive form of MKK9. Plants with constitutively active version of MKK9 accumulate more N and have higher expression of N acquisition-related genes under low N condition as compared with the inactive MKK9 plants
physiological function
MKK6 is involved in the negative regulation of anthocyanin biosynthesis in Arabidopsis thaliana. Elevated anthocyanin levels are observed in MKK6 knockout mutant plants. The expression level of MYB75 (Myb transcription factor 75), a key positive regulator of anthocyanin biosynthesis, is upregulated in MK6 mutant plants. Suppression of high sucrose-induced anthocyanin production by pathogen associated molecular pattern-triggered immunity is also dependent on MKK6
physiological function
MKKK20 phosphorylates both mitogen-activated protein kinase kinase MKK3 and MPK18. When all three kinases are combined, no synergistic effect is observed on MPK18 phosphorylation. MKKK20 acts upstream of MPK18 and MKK3. MKKK20 and MKK3 mutants are sensitive to microtubule-disrupting drugs
physiological function
mutants deficient in PBS expression have significant reductions in vegetative growth and are sensitive to calcofluor white, an inhibitor of cell wall synthesis. Mutants also lose pathogenicity and are sensitive to an osmotic stress-inducing medium containing NaCl and sorbitol. Mutants have increased resistance to the dicarboximide fungicide iprodione and the triazole fungicide tebuconazole
physiological function
quantitative trait locus Qsd2-AK at SD2 is the single major determinant explaining the difference in seed dormancy between the dormant cultivar Azumamugi (Az) and the nondormant cultivar Kanto Nakate Gold (KNG). The dormant Az allele of MKK3 is recessive, the N260T substitution in this allele decreases MKK3 kinase activity and appears to be causal for Qsd2-AK. The N260T substitution occurs in the immediate ancestor allele of the dormant allele, and the established dormant allele became prevalent in barley cultivars grown in East Asia, where the rainy season and harvest season often overlap. Germination percentage of a loss of function mutant is reduced to 23%
physiological function
the silencing of MKK5 significantly decreases the proliferation of procyclic forms of Trypanosoma brucei. In the total proteome, a general decrease in proteins related to ribosome and translation as well as down-regulation of several components of the fatty acids biosynthesis pathway are observed. In addition, alterations in the protein levels and phosphorylation of key metabolic enzymes are observed
physiological function
-
transgenic tobacco lines overexpressing MAPKK4 show a certain degree of improvement in salt tolerance, germination, and growth. NaCl inhibits growth of overexpressed line and wild-type at the seedling stage. The overexpressing line shows longer root length, higher fresh weight, and lower malondialdehyde content in transgenic lines in comparison with that in wild-type
physiological function
-
mitogen-activated protein kinase kinase VdPbs2 is a key regulator of microsclerotia formation, oxidative stress and fungicide response and plant virulence in Verticillium dahliae via regulating the activity of VdHog1, a mitogen-activated protein kinase, MAPK. VdPbs2 and VdHog1 function in a cascade that regulates microsclerotia formation and virulence, but not all VdHog1 dependent functions are VdPbs2 regulated. VdPbs2 is essential for the oxidative stress response and is required for plant infection, VdPbs2 may be involved in the penetration process during plant infection
-
physiological function
-
the mitogen-activated protein kinase kinase BOS5 is involved in regulating vegetative differentiation and virulence in Botrytis cinerea
-
physiological function
-
mitogen activated kinase kinase gene MKK5 is not essential in the pathogenic bloodstream stage of Trypanosoma brucei, no effcts on growth and virulence either in vitro or in vivo
-
physiological function
-
mitogen activated kinase kinase gene MKK1 is not essential in the pathogenic bloodstream stage of Trypanosoma brucei, no effcts on growth and virulence either in vitro or in vivo. Trypanosoma brucei MKK1 does not appear to play a significant role in flagellar biogenesis
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physiological function
-
the silencing of MKK5 significantly decreases the proliferation of procyclic forms of Trypanosoma brucei. In the total proteome, a general decrease in proteins related to ribosome and translation as well as down-regulation of several components of the fatty acids biosynthesis pathway are observed. In addition, alterations in the protein levels and phosphorylation of key metabolic enzymes are observed
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additional information
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anaphylatoxins (mainly C5a) are key players in the initiation of arthritis and utilize the MEK kinase cascade to initiate the disease process
additional information
determination of the three-dimensional structure of rice MAPKKs and MAPKs by a homology modelling approach, protein-protein docking to predict MAPKK-MAPK interactions
additional information
determination of the three-dimensional structure of rice MAPKKs and MAPKs by a homology modelling approach, protein-protein docking to predict MAPKK-MAPK interactions
additional information
determination of the three-dimensional structure of rice MAPKKs and MAPKs by a homology modelling approach, protein-protein docking to predict MAPKK-MAPK interactions
additional information
determination of the three-dimensional structure of rice MAPKKs and MAPKs by a homology modelling approach, protein-protein docking to predict MAPKK-MAPK interactions
additional information
determination of the three-dimensional structure of rice MAPKKs and MAPKs by a homology modelling approach, protein-protein docking to predict MAPKK-MAPK interactions
additional information
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installation of a cell type-specific expression system, unique in that it allows activation of MKK signaling in cells exhibiting important generalizable behaviors (e.g., cell division and fate acquisition) without the induction of cell death or additional deleterious phenotypes commonly associated with broad activation of MKKs. Determination of influence of functional docking domains of MKKs on MAPK signal output, overview
additional information
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installation of a cell type-specific expression system, unique in that it allows activation of MKK signaling in cells exhibiting important generalizable behaviors (e.g., cell division and fate acquisition) without the induction of cell death or additional deleterious phenotypes commonly associated with broad activation of MKKs. Determination of influence of functional docking domains of MKKs on MAPK signal output, overview. The D-domains of MKK7 regulate the subcellular localization of the kinase, overview
additional information
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installation of a cell type-specific expression system, unique in that it allows activation of MKK signaling in cells exhibiting important generalizable behaviors (e.g., cell division and fate acquisition) without the induction of cell death or additional deleterious phenotypes commonly associated with broad activation of MKKs. Determination of influence of functional docking domains of MKKs on MAPK signal output, overview. The D-domains of MKK9 regulate the subcellular localization of the kinase, overview
additional information
MEK2 does not affect CSFV replication after blocking the interferon-induced Janus kinase signal transducer and activator of transcription (JAK-STAT) signaling pathway by ruxolitinib, a JAK-STAT-specific inhibitor. U0126 but not PD98059 inhibits CSFV replication
additional information
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Pfnek3 is a novel dual-specificity kinase of the malarial parasite, displaying both serine/threonine and tyrosine kinase activities, even though it has a HGDLKSTN motif in the catalytic loop that resembles the consensus HRDLKxxN signature found in the serine/threonine kinases. Tyrosine phosphorylation is involved in regulation of the serine/threonine and tyrosine kinase activities of Pfnek3
additional information
the interaction between SymRK and SIP2 is conserved among legumes, interaction analysis of SIP2 and SymRK from different legume species, overview
additional information
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the interaction between SymRK and SIP2 is conserved among legumes, interaction analysis of SIP2 and SymRK from different legume species, overview
additional information
the transient state of apo npMAP2K4 exists between the canonical kinase fold and the aggregation state. The ATP molecule under physiological conditions allows the transient conformation to rapidly assume the canonical kinase fold but the depletion of ATP under conditions of low levels of bioactivity perhaps enhances the transition to the aggregation state
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D208N
mutation abolishes MAPKK activity
S222A
mutation abolishes MAPKK activity, shows a reduction in phosphorylation in response to active MAPKKK and exerts a dominant negative effect on the serum-stimulated endogenous MAPKK
C147S
90% of wild-type activity
C218S
84% of wild-type activity, mutation drastically augments the protein production and crystallographic resolution. C218S crystals grown under microgravity in a space environment yield a 1.3 A resolution structure
C218S/C276S
40% of wild-type activity
C218S/C276S/C147S
40% of wild-type activity
C218S/C276S/C147S/C296S
20% of wild-type activity
C276S
98% of wild-type activity, mutation maintains the specific activity and increases the protein yield
C296S
79% of wild-type activity, mutation maintains the specific activity and increases the protein yield
S207E/T211E
a constitutively active MKK6 mutant
S218E/S222E
site-directed mutagenesis, a constitutively active MEK1 mutant, i.e. MEK1EE
Y156F
site-directed mutagenesis, catalytically inactive mutant. The protein level of mutant MyoD-Y156F decreases compared with that of wild type but is recovered in the presence of lactacystin, a proteasome inhibitor. The low protein level of MyoD-Y156F is recovered over that of wild-type by an additional mutation at Leu164, a critical binding residue of MAFbx/AT-1, a Skp, Cullin, F-box (SCF) E3-ubiquitin ligase
N260T
substitution decreases MKK3 kinase activity and appears to be causal for quantitiative trait locus Qsd2-AK
K102R
site-directed mutagenesis, kinase inactive mutant, but slight autophosphorylation activity, the mutant strain shows a phenotype with a proliferation defect after infection of human macrophages and no or delayed lesion development in mice
K120R
generation of kinase-negative mutants of both protein kinases SymRK and SIP2 by replacing the essential Lys residue with Arg at the ATP binding site. This Lys-to-Arg substitution (SymRK-PK-KR and SIP2-KR) abolishes the kinase activity completely, but does not affect the interaction between SymRK and SIP2
S221E/T227E
OsMKK6 is made constitutively active by mutating serine and threonine to glutamic acid by site directed mutagenesis, and transformed in indica cultivar rice var. Pusa Basmati-1. The transgenic seedlings growing in 200 mM NaCl solution show increased root/shoot length and weight, less chlorophyll beaching and higher MAPK activity compared to the wild-type. Phenotypes, overview
Y117D
-
site-directed mutagenesis, the mutation leads to drastic reductions in both Pfnek3 tyrosine phosphorylation and catalytic activities
Y117E
-
site-directed mutagenesis, the mutation leads to drastic reductions in both Pfnek3 tyrosine phosphorylation and catalytic activities
Y117F
-
site-directed mutagenesis, the mutation leads to drastic reductions in both Pfnek3 tyrosine phosphorylation and catalytic activities. Reduction in tyrosine autophosphorylation is concomitant with the decrease in kinase activities for the Y117F, Y122F, and Y172F mutants
Y122D
-
site-directed mutagenesis, the mutation leads to drastic reductions in both Pfnek3 tyrosine phosphorylation and catalytic activities
Y122E
-
site-directed mutagenesis, the mutation leads to drastic reductions in both Pfnek3 tyrosine phosphorylation and catalytic activities
Y122F
-
site-directed mutagenesis, the mutation leads to drastic reductions in both Pfnek3 tyrosine phosphorylation and catalytic activities. Reduction in tyrosine autophosphorylation is concomitant with the decrease in kinase activities for the Y117F, Y122F, and Y172F mutants
Y172D
-
site-directed mutagenesis, the mutation leads to drastic reductions in both Pfnek3 tyrosine phosphorylation and catalytic activities
Y172E
-
site-directed mutagenesis, the mutation leads to drastic reductions in both Pfnek3 tyrosine phosphorylation and catalytic activities
Y172F
-
site-directed mutagenesis, the mutation leads to drastic reductions in both Pfnek3 tyrosine phosphorylation and catalytic activities. Reduction in tyrosine autophosphorylation is concomitant with the decrease in kinase activities for the Y117F, Y122F, and Y172F mutants
Y238D
-
site-directed mutagenesis, the mutation leads to drastic reductions in both Pfnek3 tyrosine phosphorylation and catalytic activities
Y238E
-
site-directed mutagenesis, the mutation leads to drastic reductions in both Pfnek3 tyrosine phosphorylation and catalytic activities
Y238F
-
site-directed mutagenesis, inactive mutant
Y286F
-
site-directed mutagenesis, inactive mutant
Y99F
-
site-directed mutagenesis, the mutation leads to drastic reductions in both Pfnek3 tyrosine phosphorylation and catalytic activities
S235E/T241E
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constitutively active kinase, MKK3-overexpressing plants, show significantly less Pseudomonas syringae growth compared with wild-type plants at 48 and 72 h after inoculation
S235E/T241E
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constitutively active kinase, MKK3-overexpressing plants, show significantly less Pseudomonas syringae growth compared with wild-type plants at 48 and 72 h after inoculation
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mkk3 knockout plants, growth of virulent Pseudomonas syringae is increased
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mkk1 single mutant appears similar to the wild-type, basal levels of MPK4 activity are not impaired in them, and MKK1 is in part functionally redundant in unchallenged plants, overview, the mkk1/2 double mutant is severely dwarfed, phenotypes of mkk1/2 are due to loss-of-function of both MKK1 and MKK2, overview. Hormone levels and growth phenotypes of mkk1/2/sid2 and mkk1/2/ein2 triple mutants, overview
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mkk1 single mutant appears similar to the wild-type, basal levels of MPK4 activity are not impaired in them, and MKK1 is in part functionally redundant in unchallenged plants, overview, the mkk1/2 double mutant is severely dwarfed, phenotypes of mkk1/2 are due to loss-of-function of both MKK1 and MKK2, overview. Hormone levels and growth phenotypes of mkk1/2/sid2 and mkk1/2/ein2 triple mutants, overview
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mkk2 single mutant appears similar to the wild-type, basal levels of MPK4 activity are not impaired in them, and MKK2 is in part functionally redundant in unchallenged plants, overview, the mkk1/2 double mutant is severely dwarfed, phenotypes of mkk1/2 are due to loss-of-function of both MKK1 and MKK2, overview. Hormone levels and growth phenotypes of mkk1/2/sid2 and mkk1/2/ein2 triple mutants, overview
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mkk2 single mutant appears similar to the wild-type, basal levels of MPK4 activity are not impaired in them, and MKK2 is in part functionally redundant in unchallenged plants, overview, the mkk1/2 double mutant is severely dwarfed, phenotypes of mkk1/2 are due to loss-of-function of both MKK1 and MKK2, overview. Hormone levels and growth phenotypes of mkk1/2/sid2 and mkk1/2/ein2 triple mutants, overview
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transgenic ProMKK3:GUS lines show basal expression in vascular tissues that is strongly induced by Pseudomonas syringae pv tomato strain DC3000 infection but not by abiotic stresses. The growth of virulent Pst DC3000 is increased in mkk3 knockout plants and decreased in MKK3-overexpressing plants, MKK3 overexpression lines show increased expression of several PR genes, phenotypes, overview
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construction of a MKK4 deletion variant
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construction of a MKK5 deletion variant
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construction of a MKK7 deletion variant
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construction of a MKK9 deletion variant
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mkk3 knockout plants, growth of virulent Pseudomonas syringae is increased
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transgenic ProMKK3:GUS lines show basal expression in vascular tissues that is strongly induced by Pseudomonas syringae pv tomato strain DC3000 infection but not by abiotic stresses. The growth of virulent Pst DC3000 is increased in mkk3 knockout plants and decreased in MKK3-overexpressing plants, MKK3 overexpression lines show increased expression of several PR genes, phenotypes, overview
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generation of a bos5 gene deletion mutant DELTAbcos5-21 by gene replacement using Agrobacterium tumefaciens strain C58C1, complementation of the bos5 deletion mutant DELTAbos5-21 pathogenicity test in cucumber leaves, the DELTAbos5-21 is unable to infect cucumber leaves at all overview
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generation of a bos5 gene deletion mutant DELTAbcos5-21 by gene replacement using Agrobacterium tumefaciens strain C58C1, complementation of the bos5 deletion mutant DELTAbos5-21 pathogenicity test in cucumber leaves, the DELTAbos5-21 is unable to infect cucumber leaves at all overview
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generation of a bos5 gene deletion mutant DELTAbcos5-21 by gene replacement using Agrobacterium tumefaciens strain C58C1, complementation of the bos5 deletion mutant DELTAbos5-21 pathogenicity test in cucumber leaves, the DELTAbos5-21 is unable to infect cucumber leaves at all overview
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generation of a cpkk1 knockout mutant, abnormal hyphae with a reduced number of septa and thinner cell walls are observed in DELTAcpkk1 mutant. The DELTAcpkk1 strain shows strong sensitivity to digestion and a low level of cell wall resistance. Phenotype, overview
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generation of a cpkk1 knockout mutant, abnormal hyphae with a reduced number of septa and thinner cell walls are observed in DELTAcpkk1 mutant. The DELTAcpkk1 strain shows strong sensitivity to digestion and a low level of cell wall resistance. Phenotype, overview
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generation of a cpkk1 knockout mutant, abnormal hyphae with a reduced number of septa and thinner cell walls are observed in DELTAcpkk1 mutant. The DELTAcpkk1 strain shows strong sensitivity to digestion and a low level of cell wall resistance. Phenotype, overview
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generation of a cpkk3 knockout mutant. Growth of DELTAcpkk3 is unaffected in either solid or liquid medium. Phenotype, overview
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generation of a cpkk3 knockout mutant. Growth of DELTAcpkk3 is unaffected in either solid or liquid medium. Phenotype, overview
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generation of a cpkk3 knockout mutant. Growth of DELTAcpkk3 is unaffected in either solid or liquid medium. Phenotype, overview
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generation of a DELTAcpkk2 knockout mutant showing a strong growth defect on solid media when compared with the control. Phenotype, overview
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generation of a DELTAcpkk2 knockout mutant showing a strong growth defect on solid media when compared with the control. Phenotype, overview
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generation of a DELTAcpkk2 knockout mutant showing a strong growth defect on solid media when compared with the control. Phenotype, overview
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overexpression of GhMKK3 enhances plant drought tolerance. Overexpression of GhMKK3 promotes abscisic acid-induced stomatal closure and decreases stomatal density. Phenotype, overview
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overexpression of GhMKK3 enhances plant drought tolerance. Overexpression of GhMKK3 promotes abscisic acid-induced stomatal closure and decreases stomatal density. Phenotype, overview
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overexpression of a constitutively active mutant of MKK4 in bronchial epithelial cell lines increases their proliferation and invasive properties
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overexpression of a constitutively active mutant of MKK4 in bronchial epithelial cell lines increases their proliferation and invasive properties
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overexpression of a constitutively active mutant of MKK4 in bronchial epithelial cell lines increases their proliferation and invasive properties
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positive regulation of SMAD3 expression is demonstrated by expression of a constitutively active ca-MEK1 construct, where the presence of ca-MEK1 results in increased SMAD3 protein expression
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silencing of MEKK-1 in betaTC-6 and human dispersed islet cells by siRNA results in protection from DETA/NO, streptozotocin, H2O2, and tunicamycin induced cell death, transient overexpression of MEKK-1 in insulin-producing cell lines RIN-5AH and betaTC-6 leads to increase in c-Jun N-terminal kinase phosphorylation and augmented cell death induced by DETA/NO, streptozotocin, and H2O2, overview
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association between -1304T>G (rs3826392) polymorphism in the promoter of MKK4 gene and the risk of sporadic colorectal cancer in a southern Chinese population
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exogenous expression in cultured mammalian cells of an MKK7-JNK fusion protein, that functions as a constitutively active form of JNK, induces phosphorylation of PER2, an essential circadian component
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construction of deletion/disruption, null, or loss-of-function mutants, which all show a phenotype with a proliferation defect after infection of human macrophages and no or delayed lesion development in mice, gene replacement method
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construction of deletion/disruption, null, or loss-of-function mutants, which all show a phenotype with a proliferation defect after infection of human macrophages and no or delayed lesion development in mice, gene replacement method
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construction of SIP2 RNA interference (RNAi) knockdown plants. Construction of plasmids that express a fusion protein between SIP2 and the N-terminal CFP (SIP2:SCFPN173). The constructs are co-expressed in Nicotiana benthamiana epidermis leaves via Agrobacterium tumefaciens-mediated transient transformation
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construction of SIP2 RNA interference (RNAi) knockdown plants. Construction of plasmids that express a fusion protein between SIP2 and the N-terminal CFP (SIP2:SCFPN173). The constructs are co-expressed in Nicotiana benthamiana epidermis leaves via Agrobacterium tumefaciens-mediated transient transformation
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expression of the neuron-specific dominant negative mitogen activated protein kinase kinase in mutant mice leads to impaired inflammatory pain and thermal hyperalgesia
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MKK4-null MEF cells, are highly susceptible to apoptosis by LY294002, paclitaxel, or serum starvation. MKK4 loss increases PTEN expression and inhibits PI3K-dependent signaling but reveals persistent AKT phosphorylation in serum-starved MKK4-null cells
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targeted deletion of the Mkk4 gene, results in early embryonic lethality, anemia, severe hemorrhaging in the liver, impaired liver formation and abnormal hepatogenesis, which correlates with significant apoptosis of liver cells, and greatly reduced thymus size. In Mkk4-/- embryonic stem cells there is no defect in p38 activation in response to a number of stresses
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targeted deletion of the Mkk4 gene, results in early embryonic lethality, anemia, severe hemorrhaging in the liver, impaired liver formation and abnormal hepatogenesis, which correlates with significant apoptosis of liver cells, and greatly reduced thymus size. In Mkk4-/- embryonic stem cells there is no defect in p38 activation in response to a number of stresses
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targeted deletion of the Mkk4 gene, results in early embryonic lethality, anemia, severe hemorrhaging in the liver, impaired liver formation and abnormal hepatogenesis, which correlates with significant apoptosis of liver cells, and greatly reduced thymus size. In Mkk4-/- embryonic stem cells there is no defect in p38 activation in response to a number of stresses
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construction of MKK4-deficient mutant mice, phenotype, overview
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construction of MKK4-deficient mutant mice, phenotype, overview
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construction of MKK4-deficient mutant mice, phenotype, overview
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construction of MKK4 gene knockout mice, that show embryonic lethality
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construction of MKK4 gene knockout mice, that show embryonic lethality
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construction of MKK7 gene knockout mice, that show embryonic lethality
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construction of MKK7 gene knockout mice, that show embryonic lethality
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exogenous expression in cultured mammalian cells of an MKK7-JNK fusion protein, that functions as a constitutively active form of JNK, induces phosphorylation of PER2, an essential circadian component
additional information
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exogenous expression in cultured mammalian cells of an MKK7-JNK fusion protein, that functions as a constitutively active form of JNK, induces phosphorylation of PER2, an essential circadian component
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contruction of OsMKK6 overexpressing transgenic lines, functional classification of upregulated and downregulated genes in the OsMKK6 overexpressing transgenic plants, overview. A final set of 316 genes shows upregulation and 198 genes show downregulation in the constitutively active OsMKK6 transgenic plants as compared with the wild-type. Comprehensive expression analysis by gene chip microarray reveal that a substantial proportion of transcription factors are expressed differentially in OsMKK6EE transgenics
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the small grain1, smg1, mutant is isolated from the japonica variety SF43 irradiated with gamma-rirradiation, and the natural mutant smg1-2 is identified from the japonica variety Nipponbare. Identification of the mutations using a map-based cloning approach, in mitogen-activated protein kinase kinase 4, OsMKK4. The mutants exhibit small and light grains, dense and erect panicles and comparatively slightly shorter plants. The short grain and panicle phenotypes of smg1 mutants are caused by a defect in cell proliferation. Mutant phenotype, overview
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construction of a catalytically inactive enzyme knockout mutant DELTAPfnek3. The truncated Pfnek3 gene, encoding a catalytically active form of Pfnek3, is cloned into the GST-encoding pGEX-6P-1 vector
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overexpression of Gab-1 in sympathetic neuronal cells leads to increased MEK and ERK activation
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overexpression in rat highly metastatic prostate cancer cell line AT6.1 significantly reduces the metastatic ability, overexpression of an inactive MKK4 in the cells leads to reduced lung metastatses and longer survival time in injected mice, overview
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construction of a stable PK-15 cell line with MEK2 knockdown by expression of specific shRNA
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construction of gene knockout mutant by cloning approximately 500 bp from the genomic regions flanking gene MKK5 (Tb927.10.5270) into plasmid pLEW13
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construction of gene knockout mutant by cloning approximately 500 bp from the genomic regions flanking gene MKK5 (Tb927.10.5270) into plasmid pLEW13
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construction of gene knockout mutants by cloning approximately 500 bp from the genomic regions flanking gene MKK1 (Tb927.3.4860) into plasmid pLEW13
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construction of gene knockout mutants by cloning approximately 500 bp from the genomic regions flanking gene MKK1 (Tb927.3.4860) into plasmid pLEW13
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construction of gene knockout mutant by cloning approximately 500 bp from the genomic regions flanking gene MKK5 (Tb927.10.5270) into plasmid pLEW13
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construction of gene knockout mutants by cloning approximately 500 bp from the genomic regions flanking gene MKK1 (Tb927.3.4860) into plasmid pLEW13
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targeted disruption of gene VdPbs2 and mutant complementation with the VdPbs2-GFP fusion construct containing the native promoter and coding region of VdPbs2
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targeted disruption of gene VdPbs2 and mutant complementation with the VdPbs2-GFP fusion construct containing the native promoter and coding region of VdPbs2
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enzyme ZmMKK1 overexpression in Arabidopsis thaliana plants enhances the tolerance to salt and drought stresses, and the expression of ROS scavenging enzyme- and ABA-related genes, such as POD, CAT, RAB18 and RD29A under salt and drought conditions. ZmMKK1-overexpressing Arabidopsis plants show enhanced sensitivity to abscisic acid in seed germination, root length and stomata aperture. ZmMKK1-overexpressing Arabidopsis improved POD and CAT activity, reduced ROS level and rate of cell death
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enzyme ZmMKK1 overexpression in Arabidopsis thaliana plants enhances the tolerance to salt and drought stresses, and the expression of ROS scavenging enzyme- and ABA-related genes, such as POD, CAT, RAB18 and RD29A under salt and drought conditions. ZmMKK1-overexpressing Arabidopsis plants show enhanced sensitivity to abscisic acid in seed germination, root length and stomata aperture. ZmMKK1-overexpressing Arabidopsis improved POD and CAT activity, reduced ROS level and rate of cell death
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A549 cells transfected with wild-type or constitutively active MEK1 cDNA, both MEK1 expressions lead to increased SMAD3 expression and ERK phosphorylation
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cloning of cotton group B MAPKK gene GhMKK3, the gene has 6 introns, sequence comparisons and phylogenetic analysis, overexpression in Nicotiana benthamiana, RNA sequencing and quantitative real-time PCR analysis. fusion Transient expression of the GFP-tagged enzyme in Nicotiana benthamiana leaves using Agrobacterium infiltration (agroinfiltration) or transiently transformed into onion epidermal cells using particle bombardment
constitutive active form of MEK1 and siRNA-targeting MEK1 cloned into MSCV-IRES-GFP vector, retrovirally transduced to HSCs and injected into sublethally irradiated RAG2-/- (CD42.2) mice
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construction of a 35S:MKK3-WT:myc expression cassette, either myc epitope-tagged wild-type MKK3 or constitutively active MKK3 are transiently expressed in Arabidopsis thaliana protoplasts, co-overexpression of MKK3 with MKK7 in ProPR1:GUS transgenic cell line, interaction analysis of MKK3 with group C MAPK kinases by yeast two-hybrid system, MKK3 and MPK7 induce the PR1 promoter, overview
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DMKK4, DNA and amino acid sequence determination
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DNA and amino acid sequence determination and analysis, expression of wild-type and mutant GST-fusion enzymes in Escherichia coli, expression of a GFP-tagged enzyme in the null mutant strain, complementation of the null mutant strain by expression of the enzyme from plasmid or by reintegration of the wild-type gene into the genomic DNA locus
expression in COS and 293 cells
expression in Escherichia coli
expression in HEK293 cells
gene At3g21220, semi-quantitative reverse transcription-PCR expression analysis, cloning and expression of the GST-fusion enzyme MKK5 in Escherichia coli strain BL21 codon plus. Recombinant overexpression of DHA-tagged MKK5 under control of the CaMV 35S promoter in either Arabidopsis thaliana Col-0 wild-type plants or mkk5 plants
gene mapkk1, recombinant plasmid ProkII-ZmMKK1 is transformed into Agrobacterium tumefaciens strain GV3101 and the transformation of Arabidopsis thaliana ecotype Col-0 is performed using the floral dip method to generate enzyme overexpressing transgenic plants, quantitative real time PCR enzyme expression analysis, recombinant expression in Escherichia coli strain TOP10
gene Mkk4, expression in ovarian cancer cell line SKOV3ip.1, that lacks endogenous MKK4, leading to a decrease in overt metastatic implants on several tissues and organs
gene MKK4, maps to chromosome 17p11.2 and encodes a 399-amino acid protein in humans spans over 120 kb and consists of 11 exons, for identification of the genetic effects of the -1304T>G polymorphism on cancer risk, a meta-analysis composed of the publications evaluating the association between the -1304T>G polymorphism and risk of cancer is performed, overview
gene MKK4, real-time RT-PCR expression analysis
gene MKK4, recombinant expression using a cell type-specific expression system is unique in that it allows activation of MKK signaling in cells exhibiting important generalizable behaviors (e.g., cell division and fate acquisition) without the induction of cell death or additional deleterious phenotypes commonly associated with broad activation of MKKs
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gene MKK5, recombinant expression using a cell type-specific expression system is unique in that it allows activation of MKK signaling in cells exhibiting important generalizable behaviors (e.g., cell division and fate acquisition) without the induction of cell death or additional deleterious phenotypes commonly associated with broad activation of MKKs
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gene MKK7, real-time RT-PCR expression analysis
gene MKK7, recombinant expression using a cell type-specific expression system is unique in that it allows activation of MKK signaling in cells exhibiting important generalizable behaviors (e.g., cell division and fate acquisition) without the induction of cell death or additional deleterious phenotypes commonly associated with broad activation of MKKs
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gene MKK9, recombinant expression using a cell type-specific expression system is unique in that it allows activation of MKK signaling in cells exhibiting important generalizable behaviors (e.g., cell division and fate acquisition) without the induction of cell death or additional deleterious phenotypes commonly associated with broad activation of MKKs
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gene OsMKK6, DNA microarray analysis in three constitutively active OsMKK6 overexpressing lines and three wild-type Pusa Basmati (PB1) plants, quantitative RT-PCR expression analysis
gene OsMKK6, recombinant expression of enzyme mutant S221E/T227E in transgenic Oryza sativa PB1 plants under the control of constitutive 35S CaMV promoter via transformation into Agrobacterium cells and subsequently into rice
gene SMG1 encoding a MKK4 (OsMKK4), recombinant enzyme expression of wild-type and smg1-1 and smg1-2 mutants in leaves of Nicotiana benthamiana via transfection with Agrobacterium tumefaciens strain EHA105
gene Tb927.10.5270, recombinant expression of MKK5 wild-type and mutant in Escherichia coli strain BL21
gene Tb927.3.4860, recombinant expression of His-tagged MKK1 wild-type and mutants in Escherichia coli strain BL21
HA-MEK1 cloned into pRevTRE, HA-tagged MEK1 expressed in HeLa cells
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isozymes MAPKK 1, DNA and amino acid sequence determination and analysis, quantitative expression analysis: the rice MAPKK isozymes are differentially regulated by cold, heat, salinity and drought stresses, sequence comparison, phylogenetic tree, overview
isozymes MAPKK 10-2, DNA and amino acid sequence determination and analysis, quantitative expression analysis: the rice MAPKK isozymes are differentially regulated by cold, heat, salinity and drought stresses, sequence comparison, phylogenetic tree, overview
isozymes MAPKK 3, DNA and amino acid sequence determination and analysis, quantitative expression analysis: the rice MAPKK isozymes are differentially regulated by cold, heat, salinity and drought stresses, sequence comparison, phylogenetic tree, overview
isozymes MAPKK 4, DNA and amino acid sequence determination and analysis, quantitative expression analysis: the rice MAPKK isozymes are differentially regulated by cold, heat, salinity and drought stresses, sequence comparison, phylogenetic tree, overview
isozymes MAPKK 6, DNA and amino acid sequence determination and analysis, quantitative expression analysis: the rice MAPKK isozymes are differentially regulated by cold, heat, salinity and drought stresses, sequence comparison, phylogenetic tree, overview
MEK1, sequence comparison
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MKK4 or XMEK2, DNA and amino acid sequence determination
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MKK4, DNA and amino acid sequence determination, the gene is located on chromosome 17
MKK6, DNA and amino acid sequence determination and analysis, expression analysis and phylogenetic tree, recombinant ectopical expression of c-Myc-tagged MKK6a, b, and c in CHSE-214 cells
open reading frames of MKK3 cloned into the plant expression vector pRT100 and fused at their C-terminal end to a c-myc epitope. Arabidopsis protoplast transient expression
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overexpression in COS cells
phylogenetic tree of kinases derived from the kinase core sequence, overview, expression as GST-fusion protein under control of the galactose-inducible GAL1 promotor in Escherichia coli, determination of 5'-end sequences
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recombinant coexpression of His6-tagged constitutively active MEK1 mutant S218E/S222E and GST-MyoD protein
recombinant expression of a fusion protein between SIP2 and the N-terminal CFP (SIP2:SCFPN173) in Nicotiana benthamiana epidermis leaves via Agrobacterium tumefaciensmediated transient transformation. Recombinant expression of polyHis- or GST-tagged wild-type and mutant enzymes in Escherichia coli. Real-time PCR expression analysis
recombinant expression of GST-tagged MEK2 mutants in Escherichia coli strain BL21(DE3) and in HEK-293T cells, GST pulldown assay on glutathione resin with recombinantly expressed FLAG-tagged E2 protein
recombinant expression of GST-tagged wild-type and mutant Pfnek3 enzymes in Escherichia coli strain BL21
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subcloned into the pET28b bacterial expression vector and expressed with a 6 x N-terminal His tag, also subcloned into pGEX 4T-3 for bacterial expression as a GST-fusion protein
transient overexpression of MEKK-1 in insulin-producing cell lines RIN-5AH and betaTC-6
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expressed in COS7 cells
isolation of cDNA
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