EC Number   |
Application |
Reference |
|---|
    2.1.1.355 | analysis |
development of a microplate biotin/avidin peptide methylation assay, which is convenient, very accurate, reproducible, and inexpensive. Because it yields quantitative results, it can be employed for a characterization of the enzymatic properties of histone lysine methyltransferases and other protein methyltransferases and is also well suited for high-throughput applications |
671291 |
| 2.1.1.355 | analysis |
sequence context of modified residue affects G9a activity and modification in the proximal amino acids influences methylation |
671979 |
| 2.1.1.355 | medicine |
G9a plays an important role in the hypoxia-induced dimethylated histone H3 lysine 9, which inhibits the expression of several genes that likely leads to solid tumor progression |
672911 |
| 2.1.1.355 | medicine |
hepatocellular tumor tissues show high levels of H3K9me3 and H3K9-specific methyltransferase ESET proteins in 23 (54.8%) and 29 (69.0%) of 42 samples, respectively. Expression levels of isoform SUV39H1 but not those of ESET are significantly correlated with H3K9me3 levels. The cumulative HCC recurrence rate is significantly higher for patients with elevated SUV39H1 expression and H3K9me3 levels |
733991 |
| 2.1.1.355 | medicine |
SUV39H1 knockdown reduces H3K9me3 levels and impairs HCC cell growth and sphere formation. The pharmacological inhibition of SUV39H1 by chaetocin results in cell growth inhibition and inducing cellular apoptosis in culture and xenograft subcutaneous tumors. 24 of 42 HCC surgical samples display high levels of SUV39H1 expression compared with corresponding nontumor tissues. Tumor tissues show high levels of H3K9me3 and H3K9-specific methyltransferase ESET proteins in 23 (54.8%) and 29 (69.0%) samples, respectively. Expression levels of SUV39H1 but not those of ESET are significantly correlated with H3K9me3 levels. The cumulative HCC recurrence rate is significantly higher for patients with elevated SUV39H1 expression and H3K9me3 levels |
733991 |
| 2.1.1.355 | medicine |
treatment with inhibitor BIX-01294 specifically decreases global H3K9Me2 level but not H3K27Me2. The inhibition of EHMT2 decreases proliferation of NB cells and induces apoptosis by increasing caspase 8/caspase 3 activity. BIX-01294 inhibits NB cell mobility and invasion accompanied with a decreased expression of the MYCN oncogene. Inhibition of EHMT2 enhances a doxorubicin induced inhibitory effect on cell proliferation and modulates global DNA methylation levels in NB cells |
733101 |
| 2.1.1.355 | more |
functions as a coactivator for nuclear receptors, cooperating synergistically with nuclear receptor coactivators glucocorticoid receptor interacting protein 1, coactivator-associated arginine methyltransferase 1, and p300 in transient transfection assays, synergy depends strongly on the arginine-specific protein methyltransferase activity of CARM1 but does not absolutely require the enzymatic activity of G9a and is specific to CARM1 and G9a among various protein methyltransferases, link between histone arginine and lysine methylation and a mechanism for controlling whether G9a functions as a corepressor or coactivator |
674770 |
| 2.1.1.355 | more |
growth factor independent 1 interacts with G9a and recruits G9a and histone deacetylase 1 to its target promoters, including the cell cycle regulator p21Cip/WAF1 and other cell cycle regulators, in order to repress transcription through histone H3(K9) dimethylation |
675958 |
