enzyme is induced by bacterial endotoxin. The enzyme catalyzes not only biosynthesis of PAF from lyso-PAF but also incorporation of arachidonoyl-CoA to produce PAF precursor membrane glycerophospholipids (lysophosphatidylcholine acyltransferase activity). Under resting conditions, the enzyme prefers arachidonoyl-CoA and contributes to membrane biogenesis. Upon acute inflammatory stimulation with lipopolysaccharide, the activated enzyme utilizes acetyl-CoA more efficiently and produces PAF
LPCAT2 also possesses lysophosphatidylcholine acyltransferase, EC: 2.3.1.23, activity that catalyzes the incorporation of arachidonoyl-CoA into membrane phosphatidylcholine
LPCAT2 also possesses lysophosphatidylcholine acyltransferase, EC: 2.3.1.23, activity that catalyzes the incorporation of arachidonoyl-CoA into membrane phosphatidylcholine
the enzyme is activated 1. by a second-order time course after stimulation with platelet-activating factor receptor, 2. by a minute-order time course after LPS stimulation in the MyD88-dependent and p38 MAPK-dependent pathway, and 3. by an hour-order time course after LPS-stimulation in the MyD88-independent and TRIF-independent pathway
enzyme is induced by bacterial endotoxin. The enzyme catalyzes not only biosynthesis of PAF from lyso-PAF but also incorporation of arachidonoyl-CoA to produce PAF precursor membrane glycerophospholipids (lysophosphatidylcholine acyltransferase activity). Under resting conditions, the enzyme prefers arachidonoyl-CoA and contributes to membrane biogenesis. Upon acute inflammatory stimulation with lipopolysaccharide, the activated enzyme utilizes acetyl-CoA more efficiently and produces PAF
LPCAT2 also possesses lysophosphatidylcholine acyltransferase, EC: 2.3.1.23, activity that catalyzes the incorporation of arachidonoyl-CoA into membrane phosphatidylcholine
LPCAT2 also possesses lysophosphatidylcholine acyltransferase, EC: 2.3.1.23, activity that catalyzes the incorporation of arachidonoyl-CoA into membrane phosphatidylcholine
the enzyme is activated 1. by a second-order time course after stimulation with platelet-activating factor receptor, 2. by a minute-order time course after LPS stimulation in the MyD88-dependent and p38 MAPK-dependent pathway, and 3. by an hour-order time course after LPS-stimulation in the MyD88-independent and TRIF-independent pathway
compound competes with acetyl-CoA for the inhibition of isoform LPCAT2 lyso-PAFAT activity and suppresses platelet-activating factor biosynthesis in mouse peritoneal macrophages stimulated with a calcium ionophore. The compound has low inhibitory effects on isoform LPCAT1 activity
derivative of a metabolite from Penicillium sp. F33 , strong inhibition. Compound also significantly suppresses the gene expression of lyso-PAF acetyltransferase/LPCAT2 in mouse bone marrow-derived macrophages stimulated by lipopolysaccharide
derivative of a metabolite from Penicillium sp. F33 , strong inhibition. Compound also significantly suppresses the gene expression of lyso-PAF acetyltransferase/LPCAT2 in mouse bone marrow-derived macrophages stimulated by lipopolysaccharide
identification of LPCAT2-specific inhibitors in order to ameliorate platelet-activating factor-related infl ammatory diseases: N-phenylmaleimide derivatives are selected from a 174000-compound library using fluorescence-based high-throughput screening followed by the evaluation of the effects on LPCAT1 and LPCAT2 activities, cell viability, and cellular platelet-activating factor production. The selected compounds have low inhibitory effects on enzyme LPCAT1 activity which is mostly expressed in the lungs where it produces platelet-activating factor, indicating that adverse effects on respiratory functions may be avoided. Structure-activity relationship, overview
identification of LPCAT2-specific inhibitors in order to ameliorate platelet-activating factor-related infl ammatory diseases: N-phenylmaleimide derivatives are selected from a 174000-compound library using fluorescence-based high-throughput screening followed by the evaluation of the effects on LPCAT1 and LPCAT2 activities, cell viability, and cellular platelet-activating factor production. The selected compounds have low inhibitory effects on enzyme LPCAT1 activity which is mostly expressed in the lungs where it produces platelet-activating factor, indicating that adverse effects on respiratory functions may be avoided. Structure-activity relationship, overview
inhibition of lipopolysaccharide-induced platelet activating factor production and gene expression of lysophosphatidylcholine acyltransferase (LPCAT2)/lyso-PAF acetyltransferase by synthetic fumigatin derivatives, compound stability and inhibitory potencies, synthesis and evaluation, overview. Dihydrofumigatin is isolated and identified from Penicillium sp. strain F33. In addition to the efficacy to inhibit the function of lyso/PAF acetyltransferase/LPCAT2, 3-hexanoyloxy-2-methoxy-5-methyl-1,4-benzoquinone, 3-decanoyloxy-2-methoxy-5-methyl-1,4-benzoquinone, and 2-methoxy-5-methyl-3-tetradecanoyloxy-1,4-benzoquinone also inhibit the expression of LPCAT2 mRNA
inhibition of lipopolysaccharide-induced platelet activating factor production and gene expression of lysophosphatidylcholine acyltransferase (LPCAT2)/lyso-PAF acetyltransferase by synthetic fumigatin derivatives, compound stability and inhibitory potencies, synthesis and evaluation, overview. Dihydrofumigatin is isolated and identified from Penicillium sp. strain F33. In addition to the efficacy to inhibit the function of lyso/PAF acetyltransferase/LPCAT2, 3-hexanoyloxy-2-methoxy-5-methyl-1,4-benzoquinone, 3-decanoyloxy-2-methoxy-5-methyl-1,4-benzoquinone, and 2-methoxy-5-methyl-3-tetradecanoyloxy-1,4-benzoquinone also inhibit the expression of LPCAT2 mRNA
the enzyme is rapidly phosphorylated after methylcarbamylplatelet-activating factor stimulation to enhance its enzymatic activity. Knockdown of PKCalpha results in significant decrease of lyso-PAFAT activation after ATP stimulation
the enzyme is rapidly phosphorylated after methylcarbamylplatelet-activating factor stimulation to enhance its enzymatic activity. Knockdown of PKCalpha results in significant decrease of lyso-PAFAT activation after ATP stimulation
the enzyme is activated 1. by a second-order time course after stimulation with platelet-activating factor receptor, 2. by a minute-order time course after LPS stimulation in the MyD88-dependent and p38 MAPK-dependent pathway, and 3. by an hour-order time course after LPS-stimulation in the MyD88-independent and TRIF-independent pathway
transcript level and enzyme activity elevated in spinal cord of experimental allergic encephalomyelitis (EAE) mice, correlation with disease severity, accumulation of platelet-activating factor dependent on the group IVA cytosolic PLA2/LysoPAFAT present in infiltrating macrophages and activated microglia
transcript level and enzyme activity elevated in spinal cord of experimental allergic encephalomyelitis (EAE) mice, correlation with disease severity, accumulation of platelet-activating factor dependent on the group IVA cytosolic PLA2/LysoPAFAT present in infiltrating macrophages and activated microglia
two entities of lyso-PAFAT belonging to the 1-acylglycerol-3-phosphate O-acyltransferase (AGPAT) family: a constitutively expressed lyso-PAFAT, LPCAT1,and an inducible lyso-PAFAT, LPCAT2. LPCAT1 is mainly expressed in the lungs and produces PAF and dipalmitoyl-phosphatidylcholine, which is a main component of a pulmonary surfactant essential for respiration. LPCAT2 is mainly expressed in inflammatory cells and also possesses biosynthetic activities for PAF and cellular membrane phosphatidylcholine
activities of phospholipase A2 and acetyl-CoA:lyso-PAF acetyltransferase (LysoPAFAT) are elevated in the spinal cord of experimental allergic encephalomyelitis (EAE) mice, an animal model for multiple sclerosis, compared with those of naive mice and correlate with disease severity
following extracellular stimulation, platelet-activating factor is rapidly biosynthesized via a remodeling pathway in inflammatory cells such as macrophages and neutrophils. In the remodeling pathway, one of the membrane phospholipids, 1-O-alkyl-2-acyl-sn-glycero-3-phosphocholine is hydrolyzed by phospholipase A2 to produce free fatty acids and lyso-PAF (1-O-alkyl-2-hydroxy-sn-glycero-3-phosphocholine). Acetyl-CoA:lyso-PAF acetyltransferase (lyso-PAFAT) subsequently converts lyso-PAF to PAF, which is rapidly degraded to lyso-PAF and acetic acid by PAF acetylhydrolases, terminating its effects
platelet-activating factor is synthesized rapidly in the remodeling pathway from its precursor membrane phospholipid, 1-O-alkyl-2-acyl-sn-glycero-3-phosphocholine, involving the enzyme
in inflammatory and allergic processes, platelet-activating factor, PAF, is biosynthesized in specific enzymatic reactions, which involve acetyl-CoA:lyso-PAF acetyltransferases
platelet-activating factor (PAF) is a potent pro-inflammatory phospholipid mediator. In response to extracellular stimuli, PAF is rapidly biosynthesized by lyso-PAF acetyltransferase. Under inflammatory conditions, LPCAT2, but not LPCAT1, is activated and upregulated to produce the platelet-activating factor
platelet-activating factor (PAF), a potent proinflammatory lipid mediator, is synthesized rapidly in response to extracellular stimuli by the activation of acetyl-CoA:lyso-PAF acetyltransferase, lyso-PAFAT. The enzyme is rapidly phosphorylated after methylcarbamylplatelet-activating factor stimulation to enhance its enzymatic activity
stimulation by either platelet-activating factor or ATP results in PKCalpha-mediated phosphorylation of the enzyme at Ser34 causing augmentation of Vmax with minimal Km change. The enzyme is rapidly phosphorylated after methylcarbamylplatelet-activating factor stimulation to enhance its enzymatic activity
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EXPRESSION
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LITERATURE
3-hexanoyloxy-2-methoxy-5-methyl-1,4-benzoquinone, 3-decanoyloxy-2-methoxy-5-methyl-1,4-benzoquinone, and 2-methoxy-5-methyl-3-tetradecanoyloxy-1,4-benzoquinone also inhibit the expression of the enzyme mRNA
fatty acid esters of fumigatin reduce lipopolysaccharide-stimulated transcription of lyso-PAF acetyltransferase/LPCAT2 mRNA in bone marrow-derived macrophages
identification of LPCAT2-specific inhibitors in order to ameliorate PAF-related inflammatory diseases, fluorescence-based high-throughput library screening
inhibitors 3-decanoyloxy-2-methoxy-5-methyl-1,4-benzoquinone and 2-methoxy-5-methyl-3-tetradecanoyloxy-1,4-benzoquinone at 2.5 mg/kg shod significant, 47.9-51.7%, inhibition in the carrageenan-induced mouse paw edema test, stronger than that of prednisolone at 10 mg/kg
Regulation of platelet-activating factor (PAF) biosynthesis via coenzyme A-independent transacylase in the macrophage cell line IC-21 stimulated with lipopolysaccharide
A single enzyme catalyzes both platelet-activating factor production and membrane biogenesis of inflammatory cells: cloning and characterization of acetyl-CoA:lyso-PAF acetyltransferase
Platelet-activating factor production in the spinal cord of experimental allergic encephalomyelitis mice via the group IVA cytosolic phospholipase A2-Lyso-PAFAT axis
Yamazaki, Y.; Yasuda, K.; Matsuyama, T.; Ishihara, T.; Higa, R.; Sawairi, T.; Yamaguchi, M.; Egi, M.; Akai, S.; Miyase, T.; Ikari, A.; Miwa, M.; Sugatani, J.
A Penicillium sp. F33 metabolite and its synthetic derivatives inhibit acetyl-CoA:1-O-alkyl-sn-glycero-3-phosphocholine acetyltransferase (a key enzyme in platelet-activating factor biosynthesis) and carrageenan-induced paw edema in mice
Rapid production of platelet-activating factor is induced by protein kinase Calpha-mediated phosphorylation of lysophosphatidylcholine acyltransferase 2 protein