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Literature summary for 2.3.1.B46 extracted from

  • Kita, Y.; Shindou, H.; Shimizu, T.
    Cytosolic phospholipase A2 and lysophospholipid acyltransferases (2019), Biochim. Biophys. Acta, 1864, 838-845 .
    View publication on PubMed
Search for more literature for 2.3.1.B46

Localization

Localization Comment Organism GeneOntology No. Textmining
membrane
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 Mus musculus 16020
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Natural Substrates/ Products (Substrates)

Natural Substrates Organism Comment (Nat. Sub.) Natural Products Comment (Nat. Pro.) Rev. Reac.
arachidonoyl-CoA + 1-acyl-lysophosphatidylinositol Mus musculus
-
 CoA + 1-acyl-2-arachidonoyl-lysophosphatidylinositol
-
 ?
eicosapentaenoyl-CoA + 1-acyl-lysophosphatidylinositol Mus musculus
-
 CoA + 1-acyl-2-eicosapentaenoyl-lysophosphatidylinositol
-
 ?
additional information Mus musculus LPIAT1 prefers 20:4-CoA and 20:5-CoA as donors ?
-
-

Organism

Organism UniProt Comment Textmining
Mus musculus Q8CHK3
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-

Substrates and Products (Substrate)

Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
arachidonoyl-CoA + 1-acyl-lysophosphatidylinositol
-
 Mus musculus CoA + 1-acyl-2-arachidonoyl-lysophosphatidylinositol
-
 ?
eicosapentaenoyl-CoA + 1-acyl-lysophosphatidylinositol
-
 Mus musculus CoA + 1-acyl-2-eicosapentaenoyl-lysophosphatidylinositol
-
 ?
additional information LPIAT1 prefers 20:4-CoA and 20:5-CoA as donors Mus musculus ?
-
-

Synonyms

Synonyms Comment Organism
LPIAT1
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 Mus musculus
LPLAT 7
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 Mus musculus
lysophosphatidylinositol-acyltransferase-1
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 Mus musculus
lysophospholipid acyltransferase 7
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 Mus musculus
MBOAT7
-
 Mus musculus

General Information

General Information Comment Organism
evolution the enzyme belongs to the MBOAT family Mus musculus
malfunction LPIAT1 deficiency induces abnormal brain morphology, delays neural migration, and reduces neurite outgrowth in mice. The size of LPIAT1-KO mice is significantly smaller than that of their littermates. The frequency of mice carrying the knockout mutation is lower than that expected by Mendelian genetics. Rs641738, a polymorphism in the LPIAT1 (MBOAT7) locus is reported to associate with hepatic inflammation and increased risk of fibrosis, nonalcoholic fatty liver disease, and alcohol related cirrhosis. This variant decreases LPIAT1 expression in the liver and changes PI compositions in the plasma. Other mutations are also reported to lead to intellectual disability, suggesting the importance of AA-containing phosphatidylinositol in the disease development Mus musculus
metabolism phospholipase A2 (PLA2) plays a role in membrane phospholipid remodeling by coupling with re-acylation processes mediated by lysophospholipid acyltransferases (LPLATs) to generate sn-1/sn-2 fatty acid asymmetry of phospholipids. Lysophospholipids are acylated by LPLAT to generate phospholipids phosphatidic acid (PA), phosphatidylcholine (PC), phosphatidylethanolamine (PE), phosphatidylserine (PS), phosphatidylinositol (PI), phosphatidylglycerol (PG), and cardiolipin (CL) by LPLATs. In the Kennedy pathway, glycerol-3-phosphate (G3P) is first acylated by glycerol-phosphate acyltransferase (GPAT) to form lyso-PA (LPA), which is subsequently converted to PA by LPA-acyltransferase (LPAAT) Mus musculus