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Literature summary 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

Activating Compound

EC Number Activating Compound Comment Organism Structure
2.3.1.23 ATP
-
 Mus musculus
2.3.1.23 lipolysaccharide
-
 Mus musculus
2.3.1.23 additional information in macrophages, extracellular stimuli such as ATP, PAF, and lipopolysaccharides phosphorylate and activate LPCAT2, but not LPCAT1 Mus musculus
2.3.1.23 PAF
-
 Mus musculus

Protein Variants

EC Number Protein Variants Comment Organism
2.3.1.23 additional information construction of LPCAT3-deficient mutant mice, phenotype, overview Mus musculus
2.3.1.23 additional information construction of two independent LPCAT1-deficient mouse lines Mus musculus
2.3.1.23 additional information construction of two independent LPCAT1-deficient mouse lines. LPCAT1-KO mice also show decreased lung dipalmitoyl-PC and blood oxygenation levels, and lower survival ratios compared to wild-type mice in a ventilator-induced lung injury model, which is an acute lung inflammatory model Mus musculus

Localization

EC Number Localization Comment Organism GeneOntology No. Textmining
2.3.1.B46 membrane
-
 Mus musculus 16020
-

Natural Substrates/ Products (Substrates)

EC Number Natural Substrates Organism Comment (Nat. Sub.) Natural Products Comment (Nat. Pro.) Rev. Reac.
2.3.1.23 arachidonoyl-CoA + 1-acyl-lysophosphatidylcholine Mus musculus preferred substrate CoA + 1-acyl-2-arachidonoyl-lysophosphatidylcholine
-
 ?
2.3.1.23 palmitoyl-CoA + 1-palmitoyl-sn-lysophosphatidylcholine Mus musculus dipalmitoyl-PC is biosynthesized by LPCAT1 in the Lands' cycle CoA + 1,2-dipalmitoyl-sn-lysophosphatidylcholine
-
 ?
2.3.1.B46 arachidonoyl-CoA + 1-acyl-lysophosphatidylinositol Mus musculus
-
 CoA + 1-acyl-2-arachidonoyl-lysophosphatidylinositol
-
 ?
2.3.1.B46 eicosapentaenoyl-CoA + 1-acyl-lysophosphatidylinositol Mus musculus
-
 CoA + 1-acyl-2-eicosapentaenoyl-lysophosphatidylinositol
-
 ?
2.3.1.B46 additional information Mus musculus LPIAT1 prefers 20:4-CoA and 20:5-CoA as donors ?
-
-

Organism

EC Number Organism UniProt Comment Textmining
2.3.1.23 Mus musculus Q3TFD2
-
-
2.3.1.23 Mus musculus Q8BYI6
-
-
2.3.1.23 Mus musculus Q91V01
-
-
2.3.1.B46 Mus musculus Q8CHK3
-
-

Posttranslational Modification

EC Number Posttranslational Modification Comment Organism
2.3.1.23 phosphoprotein in macrophages, extracellular stimuli such as ATP, PAF, and lipopolysaccharides phosphorylate and activate LPCAT2 Mus musculus

Source Tissue

EC Number Source Tissue Comment Organism Textmining
2.3.1.23 alveolar cell type II
-
 Mus musculus
-
2.3.1.23 brain
-
 Mus musculus
-
2.3.1.23 intestinal stem cell
-
 Mus musculus
-
2.3.1.23 intestine
-
 Mus musculus
-
2.3.1.23 lung mainly Mus musculus
-
2.3.1.23 macrophage
-
 Mus musculus
-
2.3.1.23 retina mainly Mus musculus
-

Substrates and Products (Substrate)

EC Number Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
2.3.1.23 arachidonoyl-CoA + 1-acyl-lysophosphatidylcholine preferred substrate Mus musculus CoA + 1-acyl-2-arachidonoyl-lysophosphatidylcholine
-
 ?
2.3.1.23 arachidonoyl-CoA + 1-acyl-lysophosphatidylethanolamine
-
 Mus musculus CoA + 1-acyl-2-arachidonoyl-lysophosphatidylethanolamine
-
 ?
2.3.1.23 arachidonoyl-CoA + 1-acyl-lysophosphatidylserine
-
 Mus musculus CoA + 1-acyl-2-arachidonoyl-lysophosphatidylserine
-
 ?
2.3.1.23 additional information LPCAT3 biosynthesizes phosphatidylcholine with arachidonic acid. LPCAT3 can also produce phosphatidylethanolamine and phosphatidylserine with arachidonic acid Mus musculus ?
-
-
2.3.1.23 additional information the enzyme Lpcat1 also shows lyso-PAF acetyltransferase activity, EC 2.3.1.67 Mus musculus ?
-
-
2.3.1.23 additional information the enzyme Lpcat2 also shows lyso-PAF acetyltransferase activity, EC 2.3.1.67 Mus musculus ?
-
-
2.3.1.23 palmitoyl-CoA + 1-palmitoyl-sn-lysophosphatidylcholine
-
 Mus musculus CoA + 1,2-dipalmitoyl-sn-lysophosphatidylcholine
-
 ?
2.3.1.23 palmitoyl-CoA + 1-palmitoyl-sn-lysophosphatidylcholine dipalmitoyl-PC is biosynthesized by LPCAT1 in the Lands' cycle Mus musculus CoA + 1,2-dipalmitoyl-sn-lysophosphatidylcholine
-
 ?
2.3.1.B46 arachidonoyl-CoA + 1-acyl-lysophosphatidylinositol
-
 Mus musculus CoA + 1-acyl-2-arachidonoyl-lysophosphatidylinositol
-
 ?
2.3.1.B46 eicosapentaenoyl-CoA + 1-acyl-lysophosphatidylinositol
-
 Mus musculus CoA + 1-acyl-2-eicosapentaenoyl-lysophosphatidylinositol
-
 ?
2.3.1.B46 additional information LPIAT1 prefers 20:4-CoA and 20:5-CoA as donors Mus musculus ?
-
-

Synonyms

EC Number Synonyms Comment Organism
2.3.1.23 LPCAT1
-
 Mus musculus
2.3.1.23 LPCAT2
-
 Mus musculus
2.3.1.23 LPCAT3
-
 Mus musculus
2.3.1.23 LPLAT
-
 Mus musculus
2.3.1.23 lyso-PAF acetyltransferase
-
 Mus musculus
2.3.1.23 lysophospholipid acyltransferase
-
 Mus musculus
2.3.1.B46 LPIAT1
-
 Mus musculus
2.3.1.B46 LPLAT 7
-
 Mus musculus
2.3.1.B46 lysophosphatidylinositol-acyltransferase-1
-
 Mus musculus
2.3.1.B46 lysophospholipid acyltransferase 7
-
 Mus musculus
2.3.1.B46 MBOAT7
-
 Mus musculus

Expression

EC Number Organism Comment Expression
2.3.1.23 Mus musculus LPCAT2 expression is increased by 16 h treatment with lipopolysaccharides up

General Information

EC Number General Information Comment Organism
2.3.1.23 evolution the enzyme belongs to the MBOAT family Mus musculus
2.3.1.23 malfunction LPCAT1 gene-trapped mice show decreased lung saturated phosphatidylcholine and higher perinatal mortality due to respiratory failure. LPCAT1-KO mice also show decreased lung dipalmitoyl-PC and blood oxygenation levels, and lower survival ratios compared to wild-type mice in a ventilator-induced lung injury model, which is an acute lung inflammatory model. Retinal degeneration and defects in visual function are also reported in a mouse strain containing a mutation in LPCAT1, rd11, reduced retinal dipalmitoyl-PC contents in mutant mice, reproducing the similar observation in the lung Mus musculus
2.3.1.23 malfunction LPCAT1 gene-trapped mice show decreased lung saturated phosphatidylcholine and higher perinatal mortality due to respiratory failure. LPCAT1-KO mice also show decreased lung dipalmitoyl-PC and blood oxygenation levels, and lower survival ratios compared to wild-type mice in a ventilator-induced lung injury model, which is an acute lung inflammatory model. Retinal degeneration and defects in visual function are also reported in a mouse strain containing a mutation in LPCAT1, reduced retinal dipalmitoyl-PC contents in mutant mice, reproducing the similar observation in the lung Mus musculus
2.3.1.23 malfunction LPCAT3 deficiency decreases arachidonic acid containing PC, PE, and PS and induces neonatal lethality due to triacylglycerol (TG) accumulation and dysfunction in enterocytes. LPCAT3-KO mice show longer and bigger small intestine. In response to high-fat feeding, LPCAT3 deficiency in the intestine increases a gut hormone, GLP-1, and oleoylethanolamide. These results suggest that AA-containing PC is a key molecule in regulating dietary lipid absorption. LPCAT3 deficiency reduces cholesterol efflux in macrophages and intestine. Excess cellular cholesterol by LPCAT3 deficiency increases intestinal stem cell proliferation and promotes tumorigenesis Mus musculus
2.3.1.23 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
2.3.1.23 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). Dipalmitoyl-PC is biosynthesized by LPCAT1 in the Lands' cycle Mus musculus
2.3.1.23 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). PAF is a potent phospholipid mediator that is biosynthesized by lyso-PAF acetyltransferase using lyso-PAF and acetyl-CoA Mus musculus
2.3.1.23 additional information a constitutive type of lyso-PAF acetyltransferase enzyme Mus musculus
2.3.1.23 additional information an inducible type of lyso-PAF acetyltransferase enzyme Mus musculus
2.3.1.23 physiological function role for LPCAT1 in respiratory function: the production of surfactant phospholipids Mus musculus
2.3.1.23 physiological function role for LPCAT3 in lipid and energy homeostasis Mus musculus
2.3.1.B46 evolution the enzyme belongs to the MBOAT family Mus musculus
2.3.1.B46 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
2.3.1.B46 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