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acyl-CoA + sn-glycerol 3-phosphate
CoA + 1-acyl-sn-glycerol 3-phosphate
acyl-CoA + sn-glycerol 3-phosphate
CoA + 1-acyl-sn-glycerol 3-phosphate
fatty acyl-CoA + glycerol-3-phosphate
CoA + lysophosphatidic acid
-
-
-
-
?
glycerol 3-phosphate + palmitoyl-CoA
CoA + 1-palmitoyl-sn-glycerol 3-phosphate
-
-
-
-
?
lauroyl-CoA + glycerol-3-phosphate
CoA + 1-lauroyl-sn-glycerol 3-phosphate
-
-
-
-
?
lauroyl-CoA + sn-glycerol 3-phosphate
CoA + 1-lauroyl-sn-glycerol 3-phosphate
-
-
-
-
?
linoleoyl-CoA + glycerol-3-phosphate
CoA + 1-linoleoyl-sn-glycerol 3-phosphate
-
-
-
-
?
oleoyl-CoA + glycerol-3-phosphate
CoA + 1-oleoyl-sn-glycerol 3-phosphate
-
-
-
-
?
palmitoyl-CoA + glycerol-3-phosphate
CoA + 1-palmitoyl-sn-glycerol 3-phosphate
-
-
-
-
?
additional information
?
-
acyl-CoA + sn-glycerol 3-phosphate
CoA + 1-acyl-sn-glycerol 3-phosphate
-
-
-
?
acyl-CoA + sn-glycerol 3-phosphate
CoA + 1-acyl-sn-glycerol 3-phosphate
-
-
-
?
acyl-CoA + sn-glycerol 3-phosphate
CoA + 1-acyl-sn-glycerol 3-phosphate
acyl-CoA specificity of GPAT1 is 16:0 > 18:0 > 18:1
-
-
?
acyl-CoA + sn-glycerol 3-phosphate
CoA + 1-acyl-sn-glycerol 3-phosphate
-
-
-
-
?
acyl-CoA + sn-glycerol 3-phosphate
CoA + 1-acyl-sn-glycerol 3-phosphate
-
-
-
?
acyl-CoA + sn-glycerol 3-phosphate
CoA + 1-acyl-sn-glycerol 3-phosphate
-
-
-
?
acyl-CoA + sn-glycerol 3-phosphate
CoA + 1-acyl-sn-glycerol 3-phosphate
-
key enzyme in de novo triacylglycerol synthesis
-
-
?
acyl-CoA + sn-glycerol 3-phosphate
CoA + 1-acyl-sn-glycerol 3-phosphate
GPAT2 shows no acyl-CoA specificity
-
-
?
acyl-CoA + sn-glycerol 3-phosphate
CoA + 1-acyl-sn-glycerol 3-phosphate
GPAT3 shows a specificity for 16:0, 18:1, 18:2 acyl-CoAs
-
-
?
acyl-CoA + sn-glycerol 3-phosphate
CoA + 1-acyl-sn-glycerol 3-phosphate
GPAT3 uses oleoyl-CoA as the preferred substrate compared to all other acyl-CoAs such as palmitoyl-CoA, myristoyl-CoA, and stearoyl-CoA
-
-
?
acyl-CoA + sn-glycerol 3-phosphate
CoA + 1-acyl-sn-glycerol 3-phosphate
GPAT4 shows no acyl-CoA specificity
-
-
?
additional information
?
-
GPAT1 preferentially catalyzes saturated fatty acids (FAs) (palmitate or C16:0) and selectively transfers acyl-CoA to the sn-1 position of glycerol 3-phosphate. Subsequently, lysophosphatidic acid, phosphatidic acid, and diacylglycerol are produced in the glycerophospholipid pathway
-
-
-
additional information
?
-
GPAT1 preferentially catalyzes saturated fatty acids (FAs) (palmitate or C16:0) and selectively transfers acyl-CoA to the sn-1 position of glycerol 3-phosphate. Subsequently, lysophosphatidic acid, phosphatidic acid, and diacylglycerol are produced in the glycerophospholipid pathway
-
-
-
additional information
?
-
GPAT1 preferentially catalyzes saturated fatty acids (FAs) (palmitate or C16:0) and selectively transfers acyl-CoA to the sn-1 position of glycerol 3-phosphate. Subsequently, lysophosphatidic acid, phosphatidic acid, and diacylglycerol are produced in the glycerophospholipid pathway
-
-
-
additional information
?
-
the isozyme GPAT3 possesses both AGPAT and GPAT activities. Microsomal GPAT3 catalyzes a broad range of reactions using long-chain acyl-CoA as substrates, including saturated and unsaturated FAs. GPAT3 uses oleoyl-CoA as the preferred substrate compared to all other acyl-CoAs such as palmitoyl-CoA, myristoyl-CoA, and stearoyl-CoA
-
-
-
additional information
?
-
the isozyme GPAT3 possesses both AGPAT and GPAT activities. Microsomal GPAT3 catalyzes a broad range of reactions using long-chain acyl-CoA as substrates, including saturated and unsaturated FAs. GPAT3 uses oleoyl-CoA as the preferred substrate compared to all other acyl-CoAs such as palmitoyl-CoA, myristoyl-CoA, and stearoyl-CoA
-
-
-
additional information
?
-
the isozyme GPAT3 possesses both AGPAT and GPAT activities. Microsomal GPAT3 catalyzes a broad range of reactions using long-chain acyl-CoA as substrates, including saturated and unsaturated FAs. GPAT3 uses oleoyl-CoA as the preferred substrate compared to all other acyl-CoAs such as palmitoyl-CoA, myristoyl-CoA, and stearoyl-CoA
-
-
-
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2-(nonylsulfonamido)benzoic acid
i.e. FSG67a, GPAT inhibitor, has a broad spectrum inhibitory effect on GPAT activity
NEM
mitochondrial GPAT2 is sensitive to NEM
(+-)-2-(2-hydroxy-3-(octylsulfonamido)-cyclopentyl)acetic acid
-
8% inhibition at 40 microg/ml
(+-)-2-hydroxy-3-(octylsulfonamido)-cyclohexanecarboxylic acid
-
36% inhibition at 40 microg/ml
(+-)-2-hydroxy-3-(octylsulfonamido)-cyclopentane carboxylic acid
-
97% inhibition at 40 microg/ml
(+-)-2-hydroxy-3-(octylsulfonamido)-cyclopentanecarboxylic acid
-
3% inhibition at 40 microg/ml
2-(2-phenylethylsulfonamido)benzoic acid
-
-
2-(4-chlorophenylsulfonamido)benzoic acid
-
-
2-(hexadecylsulfonamido)benzoic acid
-
-
2-(methylsulfonamido)benzoic acid
-
-
2-(nonylsulfonamido)benzoic acid
2-(nonylsulfonamido)benzylphosphonic acid
-
-
2-(octylsulfonamido)phenylphosphonic acid
-
-
2-(pentylsulfonamido)benzylphosphonic acid
-
-
2-(phenylmethylsulfonamido)benzoic acid
-
-
2-(phenylsulfonamido)benzoic acid
-
-
2-(tetradecylsulfonamido)benzoic acid
-
-
3-(2-phenylethylsulfonamido)benzoic acid
-
-
3-(4-chlorophenylsulfonamido)benzoic acid
-
-
3-(nonylsulfonamido)benzoic acid
-
-
3-(nonylsulfonamido)benzylphosphonic acid
-
-
3-(nonylsulfonamidomethyl)benzoic acid
-
-
3-(octylsulfonamido)phenylphosphonic acid
-
-
3-(pentylsulfonamido)benzylphosphonic acid
-
-
3-(pentylsulfonamidomethyl)benzoic acid
-
-
3-(phenylmethylsulfonamido)benzoic acid
-
-
3-(phenylsulfonamido)benzoic acid
-
-
4-(2-phenylethylsulfonamido)benzoic acid
-
-
4-(4-chlorophenylsulfonamido)benzoic acid
-
-
4-(nonylsulfonamido)benzoic acid
-
-
4-(nonylsulfonamido)benzylphosphonic acid
-
-
4-(nonylsulfonamidomethyl)benzoic acid
-
-
4-(octylsulfonamido)phenylphosphonic acid
-
-
4-(pentylsulfonamido)benzylphosphonic acid
-
-
4-(pentylsulfonamidomethyl)benzoic acid
-
-
4-(phenylmethylsulfonamido)benzoic acid
-
-
4-(phenylsulfonamido)benzoic acid
-
-
5-chloro-2-(nonylsulfonamido)benzoic acid
-
-
5-fluoro-2-(octylsulfonamido)benzoic acid
-
-
5-hydroxy-2-(octylsulfonamido)benzoic acid
-
-
2-(nonylsulfonamido)benzoic acid
-
-
2-(nonylsulfonamido)benzoic acid
-
97% inhibition at 40 microg/ml
2-(nonylsulfonamido)benzoic acid
i.e. FSG67a, GPAT inhibitor, has a broad spectrum inhibitory effect on GPAT activity
N-ethylmaleimide
-
-
NEM
-
NEM
microsomal GPAT3 activity is sensitive to NEM
additional information
mitochondrial GPAT1 is resistant to inactivation induced by sulfhydryl-group modifying reagents like N-ethylmaleimide (NEM)
-
additional information
mitochondrial GPAT1 is resistant to inactivation induced by sulfhydryl-group modifying reagents like N-ethylmaleimide (NEM)
-
additional information
mitochondrial GPAT1 is resistant to inactivation induced by sulfhydryl-group modifying reagents like N-ethylmaleimide (NEM)
-
additional information
-
cyclopentyl and cyclohexyl scaffolds may be occluded from the enzyme active site by two protein loops that sterically guard the phosphate binding region
-
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Acquired Immunodeficiency Syndrome
Mitochondrial glycerol-3-phosphate acyltransferase-1 is essential in liver for the metabolism of excess acyl-CoAs.
Breast Neoplasms
AGPAT9 suppresses cell growth, invasion and metastasis by counteracting acidic tumor microenvironment through KLF4/LASS2/V-ATPase signaling pathway in breast cancer.
Breast Neoplasms
Glycerol-3-phosphate acyltranferase-2 behaves as a cancer testis gene and promotes growth and tumorigenicity of the breast cancer MDA-MB-231 cell line.
Breast Neoplasms
Integration of metabolomics and expression of glycerol-3-phosphate acyltransferase (GPAM) in breast cancer-link to patient survival, hormone receptor status, and metabolic profiling.
Carcinogenesis
Mice Deficient in Glycerol-3-Phosphate Acyltransferase-1 Have a Reduced Susceptibility to Liver Cancer.
Carcinogenesis
Transcriptional Regulation of Acyl-CoA:Glycerol-sn-3-Phosphate Acyltransferases.
Carcinoma
Glycerol-3-phosphate Acyltransferase 1 Promotes Tumor Cell Migration and Poor Survival in Ovarian Carcinoma.
Carcinoma, Hepatocellular
An enzymatic rationale for the randomization of the positional distribution of fatty acids in phospholipids of ascites hepatoma AH 130.
Carcinoma, Hepatocellular
Anthocyanin inhibits high glucose-induced hepatic mtGPAT1 activation and prevents fatty acid synthesis through PKC{zeta}
Carcinoma, Hepatocellular
CTRP12 inhibits triglyceride synthesis and export in hepatocytes by suppressing HNF-4? and DGAT2 expression.
Carcinoma, Hepatocellular
The ménage à trois of autophagy, lipid droplets and liver disease.
Cardiovascular Diseases
Identification of a novel sn-glycerol-3-phosphate acyltransferase isoform, GPAT4, as the enzyme deficient in Agpat6-/- mice.
Choline Deficiency
Effect of methotrexate on long-chain fatty acid metabolism in liver of rats fed a standard or a defined, choline-deficient diet.
Diabetes Mellitus, Type 2
Inhibition of glycerol-3-phosphate acyltransferase as a potential treatment for insulin resistance and type 2 diabetes.
Diabetes Mellitus, Type 2
Mice deficient in mitochondrial glycerol-3-phosphate acyltransferase-1 have diminished myocardial triacylglycerol accumulation during lipogenic diet and altered phospholipid fatty acid composition.
Diabetes Mellitus, Type 2
Studies of association of AGPAT6 variants with type 2 diabetes and related metabolic phenotypes in 12,068 Danes.
Embryo Loss
Plastid lysophosphatidyl acyltransferase is essential for embryo development in Arabidopsis.
Endometritis
Genomic breeding values, SNP effects and gene identification for disease traits in cow training sets.
Fatty Liver
Glycerol-3-phosphate Acyltransferase1 Is a Model-Agnostic Node in Nonalcoholic Fatty Liver Disease: Implications for Drug Development and Precision Medicine.
Fatty Liver
Hepatic overexpression of glycerol-sn-3-phosphate acyltransferase 1 in rats causes insulin resistance.
Fatty Liver
Hepatic triacylglycerol synthesizing activity during progression of alcoholic liver injury in the baboon.
Fatty Liver
Mitochondrial glycerol-3-phosphate acyltransferase-1 is essential in liver for the metabolism of excess acyl-CoAs.
Fatty Liver
Molecular Mechanism of Age-Specific Hepatic Lipid Accumulation in PPARalpha (+/-):LDLR (+/-) Mice, an Obese Mouse Model.
Fatty Liver
Regulation of hepatic mitochondrial metabolism in response to a high fat diet: a longitudinal study in rats.
Fatty Liver
Resveratrol protects against hepatic insulin resistance in a rat's model of non-alcoholic fatty liver disease by down-regulation of GPAT-1 and DGAT2 expression and inhibition of PKC membranous translocation.
Fatty Liver
The ménage à trois of autophagy, lipid droplets and liver disease.
glycerol-3-phosphate 1-o-acyltransferase deficiency
Agpat6 deficiency causes subdermal lipodystrophy and resistance to obesity.
glycerol-3-phosphate 1-o-acyltransferase deficiency
GPAT3 deficiency alleviates insulin resistance and hepatic steatosis in a mouse model of severe congenital generalized lipodystrophy.
glycerol-3-phosphate 1-o-acyltransferase deficiency
Mitochondrial glycerol-3-phosphate acyltransferase-1 is essential for murine CD4(+) T cell metabolic activation.
Hepatomegaly
The hypolipidemic peroxisome-proliferating drug, bis(carboxymethylthio)-1.10 decane, a dicarboxylic metabolite of tiadenol, is activated to an acylcoenzyme A thioester.
Hyperlipidemias
Hepatic overexpression of glycerol-sn-3-phosphate acyltransferase 1 in rats causes insulin resistance.
Hyperlipidemias
Increased hepatic lipogenesis in insulin resistance and type 2 diabetes is associated to AMPK signaling pathway upregulation in Psammomys obesus.
Hypertriglyceridemia
Reversal of obesity-induced hypertriglyceridemia by (R)-?-lipoic acid in ZDF (fa/fa) rats.
Infections
Glycerol-3-phosphate acyltransferase 1 is essential for the immune response to infection with coxsackievirus B3 in mice.
Infections
Mycobacterium leprae promotes triacylglycerol de novo synthesis through induction of GPAT3 expression in human premonocytic THP-1 cells.
Infertility, Male
OsGPAT3 Plays a Critical Role in Anther Wall Programmed Cell Death and Pollen Development in Rice.
Insulin Resistance
Aralia cordata inhibits triacylglycerol biosynthesis in HepG2 cells.
Insulin Resistance
Early hepatic insulin resistance in mice: a metabolomics analysis.
Insulin Resistance
Glycerol-3-phosphate acyltransferase 1-deficiency in ob/ob mice diminishes hepatic steatosis but does not protect against insulin resistance or obesity.
Insulin Resistance
Glycerol-3-phosphate acyltransferase-1 regulates murine T-lymphocyte proliferation and cytokine production.
Insulin Resistance
Glycerol-3-phosphate acyltransferase-4-deficient mice are protected from diet-induced insulin resistance by the enhanced association of mTOR and rictor.
Insulin Resistance
GPAT Gene Silencing in Muscle Reduces Diacylglycerols Content and Improves Insulin Action in Diet-Induced Insulin Resistance.
Insulin Resistance
GPAT3 deficiency alleviates insulin resistance and hepatic steatosis in a mouse model of severe congenital generalized lipodystrophy.
Insulin Resistance
Hepatic overexpression of glycerol-sn-3-phosphate acyltransferase 1 in rats causes insulin resistance.
Insulin Resistance
Inhibition of glycerol-3-phosphate acyltransferase as a potential treatment for insulin resistance and type 2 diabetes.
Insulin Resistance
Lipoic acid improves hypertriglyceridemia by stimulating triacylglycerol clearance and downregulating liver triacylglycerol secretion.
Insulin Resistance
Liver-directed overexpression of mitochondrial glycerol-3-phosphate acyltransferase results in hepatic steatosis, increased triacylglycerol secretion and reduced fatty acid oxidation.
Insulin Resistance
Pharmacological glycerol-3-phosphate acyltransferase inhibition decreases food intake and adiposity and increases insulin sensitivity in diet-induced obesity.
Insulin Resistance
Prevention of hepatic steatosis and hepatic insulin resistance in mitochondrial acyl-CoA:glycerol-sn-3-phosphate acyltransferase 1 knockout mice.
Insulin Resistance
Regulation of Triglyceride Metabolism. II. Function of mitochondrial GPAT1 in the regulation of triacylglycerol biosynthesis and insulin action.
Insulin Resistance
Resveratrol protects against hepatic insulin resistance in a rat's model of non-alcoholic fatty liver disease by down-regulation of GPAT-1 and DGAT2 expression and inhibition of PKC membranous translocation.
Insulin Resistance
Thioesterase superfamily member 2 promotes hepatic insulin resistance in the setting of glycerol-3-phosphate acyltransferase 1-induced steatosis.
Lipodystrophy
Agpat6 deficiency causes subdermal lipodystrophy and resistance to obesity.
Lipodystrophy
Oligomers of the lipodystrophy protein seipin may co-ordinate GPAT3 and AGPAT2 enzymes to facilitate adipocyte differentiation.
Lipodystrophy, Congenital Generalized
Description of an AGPAT2 pathologic allelic variant in a 54-year-old Caucasian woman with Berardinelli-Seip syndrome.
Lipodystrophy, Congenital Generalized
GPAT3 deficiency alleviates insulin resistance and hepatic steatosis in a mouse model of severe congenital generalized lipodystrophy.
Liver Diseases
Exome-Wide Association Study on Alanine Aminotransferase Identifies Sequence Variants in the GPAM and APOE Associated With Fatty Liver Disease.
Liver Diseases
Glycerol-3-phosphate Acyltransferase1 Is a Model-Agnostic Node in Nonalcoholic Fatty Liver Disease: Implications for Drug Development and Precision Medicine.
Liver Diseases
Resveratrol protects against hepatic insulin resistance in a rat's model of non-alcoholic fatty liver disease by down-regulation of GPAT-1 and DGAT2 expression and inhibition of PKC membranous translocation.
Liver Diseases
The ménage à trois of autophagy, lipid droplets and liver disease.
Liver Diseases
TXNIP/VDUP1 attenuates steatohepatitis via autophagy and fatty acid oxidation.
Liver Neoplasms
Mice Deficient in Glycerol-3-Phosphate Acyltransferase-1 Have a Reduced Susceptibility to Liver Cancer.
Malaria
Characterization of the Plasmodium falciparum and P. berghei glycerol 3-phosphate acyltransferase involved in FASII fatty acid utilization in the malaria parasite apicoplast.
Mastitis
Genomic breeding values, SNP effects and gene identification for disease traits in cow training sets.
Melanoma
Glycerol-3-phosphate acyltranferase-2 behaves as a cancer testis gene and promotes growth and tumorigenicity of the breast cancer MDA-MB-231 cell line.
Neoplasm Metastasis
AGPAT9 suppresses cell growth, invasion and metastasis by counteracting acidic tumor microenvironment through KLF4/LASS2/V-ATPase signaling pathway in breast cancer.
Neoplasms
AGPAT9 suppresses cell growth, invasion and metastasis by counteracting acidic tumor microenvironment through KLF4/LASS2/V-ATPase signaling pathway in breast cancer.
Neoplasms
Glycerol-3-phosphate acyltranferase-2 behaves as a cancer testis gene and promotes growth and tumorigenicity of the breast cancer MDA-MB-231 cell line.
Neoplasms
Glycerol-3-phosphate Acyltransferase 1 Promotes Tumor Cell Migration and Poor Survival in Ovarian Carcinoma.
Neoplasms
Glycerol-3-phosphate acyltransferase 2 expression modulates cell roughness and membrane permeability: An atomic force microscopy study.
Neoplasms
Glycerol-3-phosphate acyltransferase 2 is essential for normal spermatogenesis.
Neoplasms
Liver fat content and lipid metabolism in dairy cows during early lactation and during a mid-lactation feed restriction.
Neoplasms
Short rare minisatellite variant of BORIS-MS2 is related to bladder cancer susceptibility.
Neoplasms
Small non-coding RNA landscape is modified by GPAT2 silencing in MDA-MB-231 cells.
Neoplasms
The potential of antioxidant-rich Maoberry (Antidesma bunius) extract on fat metabolism in liver tissues of rats fed a high-fat diet.
Neoplasms
TXNIP/VDUP1 attenuates steatohepatitis via autophagy and fatty acid oxidation.
Non-alcoholic Fatty Liver Disease
Anthocyanin inhibits high glucose-induced hepatic mtGPAT1 activation and prevents fatty acid synthesis through PKC{zeta}
Non-alcoholic Fatty Liver Disease
Glycerol-3-phosphate Acyltransferase1 Is a Model-Agnostic Node in Nonalcoholic Fatty Liver Disease: Implications for Drug Development and Precision Medicine.
Non-alcoholic Fatty Liver Disease
Resveratrol protects against hepatic insulin resistance in a rat's model of non-alcoholic fatty liver disease by down-regulation of GPAT-1 and DGAT2 expression and inhibition of PKC membranous translocation.
Non-alcoholic Fatty Liver Disease
The ménage à trois of autophagy, lipid droplets and liver disease.
Non-alcoholic Fatty Liver Disease
TXNIP/VDUP1 attenuates steatohepatitis via autophagy and fatty acid oxidation.
Obesity
Agpat6 deficiency causes subdermal lipodystrophy and resistance to obesity.
Obesity
Glycerol-3-phosphate acyltransferase 1-deficiency in ob/ob mice diminishes hepatic steatosis but does not protect against insulin resistance or obesity.
Obesity
Hepatic knockdown of mitochondrial GPAT1 in ob/ob mice improves metabolic profile.
Obesity
Identification of a novel sn-glycerol-3-phosphate acyltransferase isoform, GPAT4, as the enzyme deficient in Agpat6-/- mice.
Obesity
Inhibition of glycerol-3-phosphate acyltransferase as a potential treatment for insulin resistance and type 2 diabetes.
Obesity
Liver-directed overexpression of mitochondrial glycerol-3-phosphate acyltransferase results in hepatic steatosis, increased triacylglycerol secretion and reduced fatty acid oxidation.
Obesity
Mice deficient in mitochondrial glycerol-3-phosphate acyltransferase-1 have diminished myocardial triacylglycerol accumulation during lipogenic diet and altered phospholipid fatty acid composition.
Obesity
Mice Deleted for GPAT3 Have Reduced GPAT Activity in White Adipose Tissue and Altered Energy and Cholesterol Homeostasis in Diet-induced Obesity.
Obesity
Mitochondrial glycerol-3-phosphate acyltransferase-1 is essential in liver for the metabolism of excess acyl-CoAs.
Obesity
Molecular identification of microsomal acyl-CoA:glycerol-3-phosphate acyltransferase, a key enzyme in de novo triacylglycerol synthesis.
Obesity
Overexpression of mitochondrial GPAT in rat hepatocytes leads to decreased fatty acid oxidation and increased glycerolipid biosynthesis.
Obesity
Pharmacological glycerol-3-phosphate acyltransferase inhibition decreases food intake and adiposity and increases insulin sensitivity in diet-induced obesity.
Obesity
Sex and Depot Differences in ex vivo Adipose Tissue Fatty Acid Storage and Glycerol-3-phosphate acyltransferase Activity.
Obesity
Thyrotropin and obesity: increased adipose triglyceride content through glycerol-3-phosphate acyltransferase 3.
Overnutrition
Role of DNA Methylation in the Regulation of Lipogenic Glycerol-3-Phosphate Acyltransferase 1 Gene Expression in the Mouse Neonatal Liver.
Overnutrition
Thioesterase superfamily member 2 promotes hepatic insulin resistance in the setting of glycerol-3-phosphate acyltransferase 1-induced steatosis.
Sepsis
A transcriptomic signature predicting septic outcome in patients undergoing autologous stem cell transplantation.
Sepsis
Accelerated hepatic lipid synthesis in fasted septic rats.
Starvation
A study of the glycerol phosphate acyltransferase and dihydroxyacetone phosphate acyltransferase activities in rat liver mitochondrial and microsomal fractions. Relative distribution in parenchymal and non-parenchymal cells, effects of N-ethylmaleimide, palmitoyl-coenzyme A concentration, starvation, adrenalectomy and anti-insulin serum treatment.
Starvation
Effects of starvation and adrenaline on glycerophosphate acyltransferase and dihydroxy acetone phosphate acyltransferase activities in rat adipocytes.
Starvation
Glycerolipid biosynthesis in rat adipose tissue. 10. Changes during a starvation and re-feeding cycle.
Starvation
The activities of lipoprotein lipase and of enzymes involved in triacylglycerol synthesis in rat adipose tissue. Effects of starvation, dietary modification and of corticotropin injection.
Thrombosis
Diverse energy metabolism patterns in females in Neodon fuscus, Lasiopodomys brandtii, and Mus musculus revealed by comparative transcriptomics under hypoxic conditions.
Zellweger Syndrome
Deficiency of enzymes catalyzing the biosynthesis of glycerol-ether lipids in Zellweger syndrome. A new category of metabolic disease involving the absence of peroxisomes.
Zellweger Syndrome
Properties of the enzymes catalyzing the biosynthesis of lysophosphatidate and its ether analog in cultured fibroblasts from Zellweger syndrome patients and normal controls.
Please wait a moment until the data is sorted. This message will disappear when the data is sorted.
0.295
(+-)-2-(2-hydroxy-3-(octylsulfonamido)-cyclopentyl)acetic acid
Homo sapiens
-
pH not specified in the publication, temperature not specified in the publication
0.164
(+-)-2-hydroxy-3-(octylsulfonamido)-cyclohexanecarboxylic acid
Homo sapiens
-
pH not specified in the publication, temperature not specified in the publication
0.255
(+-)-2-hydroxy-3-(octylsulfonamido)-cyclopentane carboxylic acid
Homo sapiens
-
pH not specified in the publication, temperature not specified in the publication
0.324
(+-)-2-hydroxy-3-(octylsulfonamido)-cyclopentanecarboxylic acid
Homo sapiens
-
pH not specified in the publication, temperature not specified in the publication
0.152
2-(2-phenylethylsulfonamido)benzoic acid
Homo sapiens
-
-
0.107
2-(4-chlorophenylsulfonamido)benzoic acid
Homo sapiens
-
-
0.0183
2-(hexadecylsulfonamido)benzoic acid
Homo sapiens
-
-
0.132
2-(methylsulfonamido)benzoic acid
Homo sapiens
-
-
0.0247
2-(nonylsulfonamido)benzoic acid
0.0811
2-(nonylsulfonamido)benzylphosphonic acid
Homo sapiens
-
-
0.0736
2-(octylsulfonamido)phenylphosphonic acid
Homo sapiens
-
-
0.129
2-(pentylsulfonamido)benzylphosphonic acid
Homo sapiens
-
-
0.14
2-(phenylmethylsulfonamido)benzoic acid
Homo sapiens
-
-
0.146
2-(phenylsulfonamido)benzoic acid
Homo sapiens
-
-
0.0174
2-(tetradecylsulfonamido)benzoic acid
Homo sapiens
-
-
0.164
3-(2-phenylethylsulfonamido)benzoic acid
Homo sapiens
-
-
0.0757
3-(4-chlorophenylsulfonamido)benzoic acid
Homo sapiens
-
-
0.0739
3-(nonylsulfonamido)benzoic acid
Homo sapiens
-
-
0.0628
3-(nonylsulfonamido)benzylphosphonic acid
Homo sapiens
-
-
0.0835
3-(nonylsulfonamidomethyl)benzoic acid
Homo sapiens
-
-
0.0724
3-(octylsulfonamido)phenylphosphonic acid
Homo sapiens
-
-
0.141
3-(pentylsulfonamido)benzylphosphonic acid
Homo sapiens
-
-
0.31
3-(pentylsulfonamidomethyl)benzoic acid
Homo sapiens
-
-
0.178
3-(phenylmethylsulfonamido)benzoic acid
Homo sapiens
-
-
0.138
3-(phenylsulfonamido)benzoic acid
Homo sapiens
-
-
0.206
4-(2-phenylethylsulfonamido)benzoic acid
Homo sapiens
-
-
0.108
4-(4-chlorophenylsulfonamido)benzoic acid
Homo sapiens
-
-
0.0889
4-(nonylsulfonamido)benzoic acid
Homo sapiens
-
-
0.0813
4-(nonylsulfonamido)benzylphosphonic acid
Homo sapiens
-
-
0.0665 - 0.129
4-(nonylsulfonamidomethyl)benzoic acid
0.0953
4-(octylsulfonamido)phenylphosphonic acid
Homo sapiens
-
-
0.148
4-(pentylsulfonamido)benzylphosphonic acid
Homo sapiens
-
-
0.217 - 0.252
4-(pentylsulfonamidomethyl)benzoic acid
0.221
4-(phenylmethylsulfonamido)benzoic acid
Homo sapiens
-
-
0.151
4-(phenylsulfonamido)benzoic acid
Homo sapiens
-
-
0.0318
5-chloro-2-(nonylsulfonamido)benzoic acid
Homo sapiens
-
-
0.089
5-fluoro-2-(octylsulfonamido)benzoic acid
Homo sapiens
-
-
0.116
5-hydroxy-2-(octylsulfonamido)benzoic acid
Homo sapiens
-
-
0.0247
2-(nonylsulfonamido)benzoic acid
Homo sapiens
-
demonstrates the greatest inhibitory activity
0.0247
2-(nonylsulfonamido)benzoic acid
Homo sapiens
-
pH not specified in the publication, temperature not specified in the publication
0.0665
4-(nonylsulfonamidomethyl)benzoic acid
Homo sapiens
-
-
0.129
4-(nonylsulfonamidomethyl)benzoic acid
Homo sapiens
-
-
0.217
4-(pentylsulfonamidomethyl)benzoic acid
Homo sapiens
-
-
0.252
4-(pentylsulfonamidomethyl)benzoic acid
Homo sapiens
-
-
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malfunction
overexpression of GPAT1 in CHO, HEK-293 and primary rodent hepatocytes is sufficient to increase fatty acid incorporation into triglycerides and phospholipids. Knockout of GPAT1 activity in cardiomyocytes and hepatocytes increases the arachidonate and oleate content of phosphocholine and phosphoethanolamine
malfunction
the alteration of lipid composition in GPAT1-/- mice decreases the susceptibility to carcinogen-induced liver tumorigenesis. Furthermore, although the changes in cellular metabolism associated with increased GPAT1 expression lead to overall ameliorative survival in breast cancer
metabolism
relation between three isoforms GPAT1, 3, and 4 and insulin resistance, overview. GPAT1 preferentially catalyzes saturated fatty acids (FAs) (palmitate or C16:0) and selectively transfers acyl-CoA to the sn-1 position of glycerol 3-phosphate. Subsequently, lysophosphatidic acid, phosphatidic acid, and diacylglycerol are produced in the glycerophospholipid pathway. These intermediate substrates serve as the critical component of the ubiquitous biological membranes and mediate intercellular signal transduction. Mitochondrial GPAT1 is a critical regulator of triacylglycerol metabolism and systemic energy homeostasis
metabolism
relation between three isoforms GPAT1, 3, and 4 and insulin resistance, role of GPAT2 in lipid metabolism, overview
metabolism
substrate channeling in the glycerol-3-phosphate pathway regulates the synthesis, storage and secretion of glycerolipids. The successive acylation of glycerol-3-phosphate (G3P) by glycerol-3-phosphate acyltransferases and acylglycerol-3-phosphate acyltransferases produces phosphatidic acid (PA), a precursor for CDP-diacylglycerol-dependent phospholipid synthesis. PA is further dephosphorylated by LIPINs to produce diacylglycerol (DG), a substrate for the synthesis of triglyceride (TG) by DG acyltransferases and a precursor for phospholipid synthesis via the CDP-choline and CDP-ethanolamine (Kennedy) pathways. The channeling of fatty acids into TG for storage in lipid droplets and secretion in lipoproteins or phospholipids for membrane biogenesis is dependent on isoform expression, activity and localization of G3P pathway enzymes, as well as dietary and hormonal and tissue-specific factors. Mechanisms that control partitioning of substrates into lipid products of the G3P pathway, overview
physiological function
GPAT1 dictates fatty acid composition at the level of AGPATs or by acyl-chain remodeling by lysophospholipid acyltransferases (LPLATs). GPAT1 determines the metabolic fate of exogenous fatty acids
physiological function
GPATs play a pivotal role in the regulation of triglyceride and phospholipid synthesis. GPATs play a critical role in the development of obesity, hepatic steatosis, and insulin resistance. GPAT1 preferentially catalyzes saturated fatty acids (FAs) (palmitate or C16:0) and selectively transfers acyl-CoA to the sn-1 position of glycerol 3-phosphate. Subsequently, lysophosphatidic acid, phosphatidic acid, and diacylglycerol are produced in the glycerophospholipid pathway. Mitochondrial isozyme GPAT1 activity has a huge impact on the regulation of TAG synthesis, is responsible for 30-50% of the total GPAT activity in the liver and approximately 30% of the total activity in the heart. GPAT1 is regulated at the transcriptional and posttranscriptional levels, and is highly expressed in adipose tissues and liver cells. Mitochondrial GPAT1 is a critical regulator of triacylglycerol metabolism and systemic energy homeostasis
physiological function
GPATs play a pivotal role in the regulation of triglyceride and phospholipid synthesis. GPATs play a critical role in the development of obesity, hepatic steatosis, and insulin resistance. Isozyme GPAT2 is highly expressed in several cancer types (such as lung, melanoma, breast, and prostate cancer) and cancer-derived human cell lines, in which GPAT2 expression is associated with histological grading of the tumor. The expression level of GPAT2 promotes the proliferation, tumorigenicity, and migration rates of breast tumor cells
malfunction
GPAT3 overexpression in human embryonic kidney (HEK)-293 cells leads to increased incorporation of exogenous oleic acid into triacylglycerol but not into phospholipids. GPAT3 overexpression in HEK-293 cells increases phosphorylation of p70 S6 kinase and 4E-binding protein 1 in an mTOR (mammalian target of rapamycin)-dependent manner, suggesting the possible involvement of lipid intermediates of TAG synthesis, such as lysophosphatidic acid and phosphatidic acid (PA), in the mTOR pathway
malfunction
-
enzyme deficiency results in an inherent defect in Jurkat T cell function and glycerophospholipid composition
malfunction
knockdown of GPAT3 and 4 almost completely prevents the formation of lipid droplets. Deficiency of GPAT greatly reduces TAG synthesis and impairs adipogenesis
malfunction
overexpression of endoplasmic reticulum-localized GPAT3 or GPAT4 in cultured cells does not affect incorporation of exogenous fatty acids into the major phospholipid classes
metabolism
relation between three isoforms GPAT1, 3, and 4 and insulin resistance, overview. GPAT3 and GPAT4 enzyme activity can be regulated by insulin upon phosphorylation at the Thr and Ser residues
metabolism
substrate channeling in the glycerol-3-phosphate pathway regulates the synthesis, storage and secretion of glycerolipids. The successive acylation of glycerol-3-phosphate (G3P) by glycerol-3-phosphate acyltransferases and acylglycerol-3-phosphate acyltransferases produces phosphatidic acid (PA), a precursor for CDP-diacylglycerol-dependent phospholipid synthesis. PA is further dephosphorylated by LIPINs to produce diacylglycerol (DG), a substrate for the synthesis of triglyceride (TG) by DG acyltransferases and a precursor for phospholipid synthesis via the CDP-choline and CDP-ethanolamine (Kennedy) pathways. The channeling of fatty acids into TG for storage in lipid droplets and secretion in lipoproteins or phospholipids for membrane biogenesis is dependent on isoform expression, activity and localization of G3P pathway enzymes, as well as dietary and hormonal and tissue-specific factors. Mechanisms that control partitioning of substrates into lipid products of the G3P pathway, overview
physiological function
in contrast to other GPATs, GPAT4 overexpression does not increase incorporation of exogenous fatty acids into triacylglycerol in HEK-293 and COS-7 cells, suggesting that lysophosphatidic acid and phosphatidic acid produced from the GPAT4 pathway may consist of a separate pool from that utilized for triacylglycerol synthesis
physiological function
GPATs play a pivotal role in the regulation of triglyceride and phospholipid synthesis. GPATs play a critical role in the development of obesity, hepatic steatosis, and insulin resistance. GPAT3 play a crucial role in lipid formation. GPAT3 plays a critical role in regulating glucose, energy, and lipid homeostasis
physiological function
GPATs play a pivotal role in the regulation of triglyceride and phospholipid synthesis. GPATs play a critical role in the development of obesity, hepatic steatosis, and insulin resistance. GPAT4 is a positive regulator of body weight
physiological function
isozyme GPAT3 is primarily involved in triglyceride (TG) storage in adipocytes. Contribution of GPATs to acyl-CoA partitioning into glycerolipid synthesis and beta-oxidation, overview
physiological function
isozyme GPAT4 is a primary contributor to lysophosphatidic acid synthesis in liver and brown adipose tissue. Contribution of GPATs to acyl-CoA partitioning into glycerolipid synthesis and beta-oxidation
additional information
the GPAT/AGPAT family acyltransferases contain four well-conserved domains (motif I-IV), which catalyze the transferase reaction and are involved in binding to the substrate (acyl acceptor, e.g., G3P)
additional information
the GPAT/AGPAT family acyltransferases contain four well-conserved domains (motif I-IV), which catalyze the transferase reaction and are involved in binding to the substrate (acyl acceptor, e.g., G3P)
additional information
the GPAT/AGPAT family acyltransferases contain four well-conserved domains (motif I-IV), which catalyze the transferase reaction and are involved in binding to the substrate (acyl acceptor, e.g., G3P)
additional information
the N-terminal domain of GPAT2 associates with the active site, which possesses the maximum homology to that of GPAT1. The GPAT/AGPAT family acyltransferases contain four well-conserved domains (motif I-IV), which catalyze the transferase reaction and are involved in binding to the substrate (acyl acceptor, e.g. G3P). The motif IV of GPAT2 is restricted to the mitochondrial membrane, but the remaining acyltransferase motifs are exposed to the cytoplasmic side of the mitochondria
additional information
the N-terminal domain of GPAT2 associates with the active site, which possesses the maximum homology to that of GPAT1. The GPAT/AGPAT family acyltransferases contain four well-conserved domains (motif I-IV), which catalyze the transferase reaction and are involved in binding to the substrate (acyl acceptor, e.g. G3P). The motif IV of GPAT2 is restricted to the mitochondrial membrane, but the remaining acyltransferase motifs are exposed to the cytoplasmic side of the mitochondria
additional information
the N-terminal domain of GPAT2 associates with the active site, which possesses the maximum homology to that of GPAT1. The GPAT/AGPAT family acyltransferases contain four well-conserved domains (motif I-IV), which catalyze the transferase reaction and are involved in binding to the substrate (acyl acceptor, e.g. G3P). The motif IV of GPAT2 is restricted to the mitochondrial membrane, but the remaining acyltransferase motifs are exposed to the cytoplasmic side of the mitochondria
additional information
the GPAT/AGPAT family acyltransferases contain four well-conserved domains (motif I-IV), which catalyze the transferase reaction and are involved in binding to the substrate (acyl acceptor, e.g., G3P). GPAT3 probably contains two transmembrane domains, and the active site of GPAT3 is located in the N-terminal domain
additional information
the GPAT/AGPAT family acyltransferases contain four well-conserved domains (motif I-IV), which catalyze the transferase reaction and are involved in binding to the substrate (acyl acceptor, e.g., G3P). GPAT3 probably contains two transmembrane domains, and the active site of GPAT3 is located in the N-terminal domain
additional information
the GPAT/AGPAT family acyltransferases contain four well-conserved domains (motif I-IV), which catalyze the transferase reaction and are involved in binding to the substrate (acyl acceptor, e.g., G3P). GPAT3 probably contains two transmembrane domains, and the active site of GPAT3 is located in the N-terminal domain
additional information
the GPAT/AGPAT family acyltransferases contain four wellconserved domains (motif I-IV), which catalyze the transferase reaction and are involved in binding to the substrate (acyl acceptor, e.g. G3P). GPAT4 possesses a series of membrane insertion helices which form hairpin loops in the membrane or monolayer. The active acyltransferase domain is located close to the C-terminus
additional information
the GPAT/AGPAT family acyltransferases contain four wellconserved domains (motif I-IV), which catalyze the transferase reaction and are involved in binding to the substrate (acyl acceptor, e.g. G3P). GPAT4 possesses a series of membrane insertion helices which form hairpin loops in the membrane or monolayer. The active acyltransferase domain is located close to the C-terminus
additional information
the GPAT/AGPAT family acyltransferases contain four wellconserved domains (motif I-IV), which catalyze the transferase reaction and are involved in binding to the substrate (acyl acceptor, e.g. G3P). GPAT4 possesses a series of membrane insertion helices which form hairpin loops in the membrane or monolayer. The active acyltransferase domain is located close to the C-terminus
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Cao, J.; Li, J.L.; Li, D.; Tobin, J.F.; Gimeno, R.E.
Molecular identification of microsomal acyl-CoA:glycerol-3-phosphate acyltransferase, a key enzyme in de novo triacylglycerol synthesis
Proc. Natl. Acad. Sci. USA
103
19695-19700
2006
Homo sapiens, Mus musculus
brenda
Chen, Y.Q.; Kuo, M.S.; Li, S.; Bui, H.H.; Peake, D.A.; Sanders, P.E.; Thibodeaux, S.J.; Chu, S.; Qian, Y.W.; Zhao, Y.; Bredt, D.S.; Moller, D.E.; Konrad, R.J.; Beigneux, A.P.; Young, S.G.; Cao, G.
AGPAT6 is a novel microsomal glycerol-3-phosphate acyltransferase
J. Biol. Chem.
283
10048-10057
2008
Homo sapiens
brenda
Takeuchi, K.; Reue, K.
Biochemistry, physiology, and genetics of GPAT, AGPAT, and lipin enzymes in triglyceride synthesis
Am. J. Physiol. Endocrinol. Metab.
296
E1195-E1209
2009
Rattus norvegicus, Rattus norvegicus (P97564), Mus musculus (Q14DK4), Mus musculus (Q61586), Mus musculus (Q8C0N2), Mus musculus (Q8K2C8), Mus musculus, Homo sapiens (Q53EU6), Homo sapiens (Q86UL3), Homo sapiens
brenda
Wydysh, E.A.; Medghalchi, S.M.; Vadlamudi, A.; Townsend, C.A.
Design and synthesis of small molecule glycerol 3-phosphate acyltransferase inhibitors
J. Med. Chem.
52
3317-3327
2009
Homo sapiens
brenda
Wydysh, E.A.; Vadlamudi, A.; Medghalchi, S.M.; Townsend, C.A.
Design, synthesis, and biological evaluation of conformationally constrained glycerol 3-phosphate acyltransferase inhibitors
Bioorg. Med. Chem.
18
6470-6479
2010
Homo sapiens, Cucurbita moschata (P10349)
brenda
Faris, R.; Weber, M.M.; Seeger, D.R.; Cavazos, D.; de Graffenried, L.; Murphy, E.J.; Jolly, C.A.
Mitochondrial glycerol-3-phosphate acyltransferase-dependent phospholipid synthesis modulates phospholipid mass and IL-2 production in Jurkat T cells
Lipids
51
291-301
2016
Homo sapiens
brenda
Lee, J.; Ridgway, N.
Substrate channeling in the glycerol-3-phosphate pathway regulates the synthesis, storage and secretion of glycerolipids
Biochim. Biophys. Acta
1865
158438
2020
Mus musculus (Q14DK4), Mus musculus (Q61586), Mus musculus (Q8C0N2), Mus musculus (Q8K2C8), Homo sapiens (Q53EU6), Homo sapiens (Q6NUI2), Homo sapiens (Q86UL3), Homo sapiens (Q9HCL2)
brenda
Yu, J.; Loh, K.; Song, Z.Y.; Yang, H.Q.; Zhang, Y.; Lin, S.
Update on glycerol-3-phosphate acyltransferases the roles in the development of insulin resistance
Nutr. Diabetes
8
34
2018
Mus musculus (Q14DK4), Mus musculus (Q61586), Mus musculus (Q8C0N2), Mus musculus (Q8K2C8), Homo sapiens (Q53EU6), Homo sapiens (Q86UL3), Homo sapiens (Q9HCL2), Mus musculus C57BL/6J (Q8K2C8)
brenda