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C211F
C211 is essential for activity
C211R
C211 is essential for activity
C211S
C211 is essential for activity
D31A
site-directed mutagenesis, construction of mutant endothelial cells via lentivirus transfection
H26A
site-directed mutagenesis, construction of mutant endothelial cells via lentivirus transfection
M427T
naturally occuring mutation, does not significantly affect the activity or function
N213A
putative N-glycosylation site
C47S
site-directed mutagenesis, construction of mutant endothelial cells via lentivirus transfection. The C47S mutant protein does not express peroxidase activity, but both PLA2 and LPCAT activities are preserved
D140A
site-directed mutagenesis, construction of mutant endothelial cells via lentivirus transfection. The D140A mutant protein retains full peroxidase activity
D31A
site-directed mutagenesis, construction of mutant endothelial cells via lentivirus transfection, the mutant loses almost all LPCAT activity, but retains PLA2 activity
H129A
site-directed mutagenesis, mutation of a residue in AGPAT motif I (HxxxxD), the mutant shows no LPEAT activity
H26A
site-directed mutagenesis, breeding of H26A Prdx6 knock-in mutant mice, the final targeting construct is linearized, sequence verified, and electroporated into C57Bl/6J ES cells (EAP6 ES cells) for insertion of the mutant sequences into the mouse genome by homologous recombination, positive clones are used for blastocyst injection into CD-1/BALB/c mice, chimeric H26A Prdx6 mice are bred to C57Bl/6J wild-type mice and the resulting heterozygotic mice are bred to homozygosity. The H26A mutant retains the ability to reduce short chain hydroperoxides, but cannot reduce phospholipid hydroperoxides, as they do not bind to the phospholipid substrate
S32A
site-directed mutagenesis, the S32A mutant retains the ability to reduce short chain hydroperoxides, but cannot reduce phospholipid hydroperoxides, as they do not bind to the phospholipid substrate
C47S
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site-directed mutagenesis, construction of mutant endothelial cells via lentivirus transfection. The C47S mutant protein does not express peroxidase activity, but both PLA2 and LPCAT activities are preserved
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D140A
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site-directed mutagenesis, construction of mutant endothelial cells via lentivirus transfection. The D140A mutant protein retains full peroxidase activity
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D31A
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site-directed mutagenesis, construction of mutant endothelial cells via lentivirus transfection, the mutant loses almost all LPCAT activity, but retains PLA2 activity
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H26A
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site-directed mutagenesis, breeding of H26A Prdx6 knock-in mutant mice, the final targeting construct is linearized, sequence verified, and electroporated into C57Bl/6J ES cells (EAP6 ES cells) for insertion of the mutant sequences into the mouse genome by homologous recombination, positive clones are used for blastocyst injection into CD-1/BALB/c mice, chimeric H26A Prdx6 mice are bred to C57Bl/6J wild-type mice and the resulting heterozygotic mice are bred to homozygosity. The H26A mutant retains the ability to reduce short chain hydroperoxides, but cannot reduce phospholipid hydroperoxides, as they do not bind to the phospholipid substrate
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additional information
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in a human hepatoma Huh7 cells, RNA interference-mediated knockdown of LPCAT3 results in virtually complete loss of membrane LPCAT activity, suggesting that LPCAT3 is primarily responsible for hepatic LPCAT activity
additional information
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membranes from HEK293 cells overexpressing LPCAT3 show significantly increased LPCAT activity as assessed by thin layer chromatography analysis with substrate preference toward unsaturated fatty acids
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enzyme LPCAT3 gene silencing by siRNA
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enzyme LPCAT3 gene silencing by siRNA
additional information
LPCAT3 isozyme knockdown to about 25% activity in U-937 cells by siRNA. LPCAT3 siRNA-transfected cells show a spindle-shaped. morphology similar to that of M1-polarized macrophages, whereas control siRNAtransfected cells show a rounded morphology typical ofM2-polarized macrophages. Knockdown of LPCAT3 in phorbol ester-treated U-937 cells decreases LPCAT activity toward linoleoyl-CoA and arachidonoyl-CoA
additional information
construction of LPCAT1 knockout HeLa cells
additional information
construction of a LPCAT knockout mutant
additional information
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construction of a LPCAT knockout mutant
additional information
construction of LPCAT1 knockout mice
additional information
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construction of LPCAT1 knockout mice
additional information
construction of LPCAT3-deficient mutant mice, phenotype, overview
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construction of LPCAT3-deficient mutant mice, phenotype, overview
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construction of LPCAT3-deficient mutant mice, phenotype, overview
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construction of two independent LPCAT1-deficient mouse lines
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construction of two independent LPCAT1-deficient mouse lines
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construction of two independent LPCAT1-deficient mouse lines
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
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
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
additional information
enzyme knockout in Neuro 2A cells via expression of mLPEAT2-siRNA
additional information
isozyme LPCAT4 is silenced in in ATDC5 cells, ATDC5 cells are transfected with LPCAT4 siRNA. LPCAT4 siRNA-transfected cells maintain viability 24 h after transfection. The transfected ATDC5 cells are cultured in alpha-MEM with ascorbic acid and ITS to induce chondrogenic differentiation. LPCAT4 siRNA transfection specifically suppresses mRNA expression of LPCAT4, without affecting LPCAT1-3 transcript levels, on day 15 after transfection. In control siRNA-transfected cells, LPCAT4 transcripts increase during chondrogenic differentiation. Knockdown of LPCAT4 does not change LPCAT enzymatic activity and the percentage of phosphatidylcholine species. Knockdown of LPCAT4 suppressed the mRNA expression of the chondrogenic differentiation markers, Col10, ALP, aggrecan, and TGF-beta and protein expression of Col10 on day 15 after transfection. The expression of Col2, Sox9, and Runx2 does not change. The knockdown of LPCAT4 suppresses the mRNA expression of BMP2, BMP6, and BMP7 during chondrogenic differentiation of ATDC5 cells
additional information
transient liver-specific knockdown of LPCAT3 in mice affecting PPARdelta-mediated activation of several hepatic genes involving in fatty acid metabolism, phenotype, overview
additional information
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transient liver-specific knockdown of LPCAT3 in mice affecting PPARdelta-mediated activation of several hepatic genes involving in fatty acid metabolism, phenotype, overview
additional information
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construction of a LPCAT knockout mutant
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additional information
recombinant expression of Arabidopsis thaliana LPCAT2, differences in incorporation of [14C]oleoyl-CoA into PtdCho in microsomal preparations of ale1 yeast expressing AtLPCAT2 with and without DTNB, overview