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acyl-CoA + 1-acyl-sn-glycerol 3-phosphate
CoA + 1,2-diacyl-sn-glycerol 3-phosphate
(5Z,8Z,11Z,14Z)-eicosatetraenoyl-CoA + 1-acyl-lysophosphatidic acid
CoA + 1-acyl-2-(5Z,8Z,11Z,14Z)-eicosatetraenoyl-lysophosphatidic acid
-
-
-
?
acyl-CoA + 1-acyl-lysophosphatidic acid
CoA + 1,2-diacyl-lysophosphatidic acid
acyl-CoA + 1-acyl-sn-glycerol 3-phosphate
CoA + 1,2-diacyl-sn-glycerol 3-phosphate
acyl-CoA + 1-oleoyl-sn-glycerol 3-phosphate
CoA + 2-acyl-1-oleoyl-sn-glycerol 3-phosphate
-
-
?
alpha-linolenoyl-CoA + 1-acyl-lysophosphatidic acid
CoA + 1-acyl-2-alpha-linolenoyl-lysophosphatidic acid
-
-
-
?
arachidonoyl-CoA + 1-acyl-sn-glycerol 3-phosphate
CoA + 1-acyl-2-arachidonoyl-sn-glycerol 3-phosphate
-
-
?
arachidonoyl-CoA + 1-oleoyl-glycerol-3-phosphate
1-oleoyl-2-arachidonoyl-glycerol-3-phosphate + CoA
-
-
-
-
?
arachidonoyl-CoA + 1-oleoyl-sn-glycerol 3-phosphate
CoA + 1-oleoyl-2-arachidonoyl-sn-glycerol 3-phosphate
about half of the rate with oleoyl-CoA
-
-
?
arachidoyl-CoA + 1-acyl-sn-glycerol 3-phosphate
CoA + 1-acyl-2-arachidoyl-sn-glycerol 3-phosphate
-
-
?
heptadecanoyl-CoA + 1-oleoyl-sn-glycerol 3-phosphate
CoA + 1-oleoyl-2-heptadecanoyl-sn-glycerol 3-phosphate
lauroyl-CoA + 1-acyl-sn-glycerol 3-phosphate
CoA + 1-acyl-2-lauroyl-sn-glycerol 3-phosphate
-
-
?
lignoceroyl-CoA + 1-acyl-sn-glycerol 3-phosphate
CoA + 1-acyl-2-lignoceroyl-sn-glycerol 3-phosphate
-
-
?
linolenoyl-CoA + 1-acyl-sn-glycerol 3-phosphate
CoA + 1-acyl-2-linolenoyl-sn-glycerol 3-phosphate
-
-
?
linoleoyl-CoA + 1-acyl-lysophosphatidic acid
CoA + 1-acyl-2-linoleoyl-lysophosphatidic acid
-
-
-
?
linoleoyl-CoA + 1-acyl-sn-glycerol 3-phosphate
CoA + 1-acyl-2-linoleoyl-sn-glycerol 3-phosphate
-
-
?
linoleoyl-CoA + 1-oleoyl-sn-glycerol 3-phosphate
CoA + 1-oleoyl-2-linoleoyl-sn-glycerol 3-phosphate
myristoyl-CoA + 1-acyl-lysophosphatidic acid
CoA + 1-acyl-2-myristoyl-lysophosphatidic acid
-
-
-
?
myristoyl-CoA + 1-acyl-sn-glycerol 3-phosphate
CoA + 1-acyl-2-myristoyl-sn-glycerol 3-phosphate
-
-
?
myristoyl-CoA + 1-oleoyl-sn-glycerol 3-phosphate
CoA + 1-oleoyl-2-myristoyl-sn-glycerol 3-phosphate
-
about 25% of the activity with oleoyl-CoA by AGPAT10/GPAT3
-
-
?
oleoyl-CoA + 1-acyl-lysophosphatidic acid
CoA + 1-acyl-2-oleoyl-lysophosphatidic acid
-
-
-
?
oleoyl-CoA + 1-acyl-sn-glycerol 3-phosphate
CoA + 1-acyl-2-oleoyl-sn-glycerol 3-phosphate
-
-
?
oleoyl-CoA + 1-oleoyl-2-lysophosphatidylcholine
CoA + 1,2-dioleoyl-sn-glycero-3-phosphocholine
-
about 10% of the activity with 1-oleoyl-2-lysophopshatidic acid by AGPAT10/GPAT3
-
-
?
oleoyl-CoA + 1-oleoyl-2-lysophosphatidylethanolamine
CoA + 1,2-dioleoyl-sn-glycero-3-phosphoethanolamine
-
about 10% of the activity with 1-oleoyl-2-lysophopshatidic acid by AGPAT10/GPAT3
-
-
?
oleoyl-CoA + 1-oleoyl-2-lysophosphatidylglycerol
CoA + 1,2-dioleoyl-sn-glycero-3-phosphate
-
about 10% of the activity with 1-oleoyl-2-lysophopshatidic acid by AGPAT10/GPAT3
-
-
?
oleoyl-CoA + 1-oleoyl-2-lysophosphatidylinositol
CoA + 1,2-dioleoyl-sn-phosphatidylinositol
oleoyl-CoA + 1-oleoyl-2-lysophosphatidylserine
CoA + 1,2-dioleoyl-sn-glycerol-3-phospho-L-serine
-
about 10% of the activity with 1-oleoyl-2-lysophopshatidic acid by AGPAT10/GPAT3
-
-
?
oleoyl-CoA + 1-oleoyl-sn-glycerol 3-phosphate
CoA + 1,2-dioleoyl-sn-glycerol 3-phosphate
oleoyl-CoA + 1-oleoyl-sn-glycerol-3-phosphate
CoA + 1,2-dioleoyl-sn-glycerol 3-phosphate
palmitoleoyl-CoA + 1-acyl-lysophosphatidic acid
CoA + 1-acyl-2-palmitoleoyl-lysophosphatidic acid
-
-
-
?
palmitoleoyl-CoA + 1-acyl-sn-glycerol 3-phosphate
CoA + 1-acyl-2-palmitoleoyl-sn-glycerol 3-phosphate
palmitoleoyl-CoA is a good substrate
-
?
palmitoyl-CoA + 1-acyl-lysophosphatidic acid
CoA + 1-acyl-2-palmitoyl-lysophosphatidic acid
-
-
-
?
palmitoyl-CoA + 1-acyl-sn-glycerol 3-phosphate
CoA + 1-acyl-2-palmitoyl-sn-glycerol 3-phosphate
palmitoyl-CoA + 1-oleoyl-sn-glycerol 3-phosphate
CoA + 1-oleoyl-2-palmitoyl-sn-glycerol 3-phosphate
pentadecanoyl-CoA + 1-oleoyl-sn-glycerol 3-phosphate
CoA + 1-oleoyl-2-pentadecanoyl-sn-glycerol 3-phosphate
stearoyl-CoA + 1-acyl-lysophosphatidic acid
CoA + 1-acyl-2-stearoyl-lysophosphatidic acid
-
-
-
?
stearoyl-CoA + 1-acyl-sn-glycerol 3-phosphate
CoA + 1-acyl-2-stearoyl-sn-glycerol 3-phosphate
-
-
?
stearoyl-CoA + 1-oleoyl-sn-glycerol 3-phosphate
CoA + 1-oleoyl-2-stearoyl-sn-glycerol 3-phosphate
additional information
?
-
acyl-CoA + 1-acyl-sn-glycerol 3-phosphate
CoA + 1,2-diacyl-sn-glycerol 3-phosphate
-
-
-
?
acyl-CoA + 1-acyl-sn-glycerol 3-phosphate
CoA + 1,2-diacyl-sn-glycerol 3-phosphate
the enzyme catalyzes the transfer of the fatty acid from an acyl donor to the sn-2-position of lysophosphatidic acid
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-
?
acyl-CoA + 1-acyl-lysophosphatidic acid
CoA + 1,2-diacyl-lysophosphatidic acid
-
-
-
?
acyl-CoA + 1-acyl-lysophosphatidic acid
CoA + 1,2-diacyl-lysophosphatidic acid
AGPAT1 and 2 show strict acyl acceptor specificity for lysophosphatidic acid, acyl-CoA specificity, overview
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?
acyl-CoA + 1-acyl-sn-glycerol 3-phosphate
CoA + 1,2-diacyl-sn-glycerol 3-phosphate
-
-
-
?
acyl-CoA + 1-acyl-sn-glycerol 3-phosphate
CoA + 1,2-diacyl-sn-glycerol 3-phosphate
-
-
-
-
?
acyl-CoA + 1-acyl-sn-glycerol 3-phosphate
CoA + 1,2-diacyl-sn-glycerol 3-phosphate
-
-
?
acyl-CoA + 1-acyl-sn-glycerol 3-phosphate
CoA + 1,2-diacyl-sn-glycerol 3-phosphate
-
-
-
?
acyl-CoA + 1-acyl-sn-glycerol 3-phosphate
CoA + 1,2-diacyl-sn-glycerol 3-phosphate
-
-
-
?
acyl-CoA + 1-acyl-sn-glycerol 3-phosphate
CoA + 1,2-diacyl-sn-glycerol 3-phosphate
-
reduction in AGPAT2 activity underlies the loss of adipose tissue in congenital generalized lipodystrophy
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-
?
acyl-CoA + 1-acyl-sn-glycerol 3-phosphate
CoA + 1,2-diacyl-sn-glycerol 3-phosphate
AGPAT2 catalyzes acylation of lysophosphatidic acid to phosphatidic acid, a precursor for both triacylglycerol and phospholipid synthesis, isozyme AGPAT2 plays a regulatory role in adipocyte differentiation
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-
?
acyl-CoA + 1-acyl-sn-glycerol 3-phosphate
CoA + 1,2-diacyl-sn-glycerol 3-phosphate
-
the enzyme catalyzes the transfer of the fatty acid from an acyl donor to the sn-2-position of lysophosphatidic acid
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-
?
acyl-CoA + 1-acyl-sn-glycerol 3-phosphate
CoA + 1,2-diacyl-sn-glycerol 3-phosphate
activity and expression pattern of AGPAT9 in lung and spleen implicates role in the biosynthesis of phospholipids and triglycerides in these tissues
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-
?
acyl-CoA + 1-acyl-sn-glycerol 3-phosphate
CoA + 1,2-diacyl-sn-glycerol 3-phosphate
acylation of lysophosphatidic acid to phosphatidic acid, precursor for triacylglycerol and phospholipid synthesis
-
-
?
acyl-CoA + 1-acyl-sn-glycerol 3-phosphate
CoA + 1,2-diacyl-sn-glycerol 3-phosphate
cloning and characterization of isoform AGPAT9
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-
?
acyl-CoA + 1-acyl-sn-glycerol 3-phosphate
CoA + 1,2-diacyl-sn-glycerol 3-phosphate
-
substrate preference analyzed, assays performed with different acyl donors
-
-
?
heptadecanoyl-CoA + 1-oleoyl-sn-glycerol 3-phosphate
CoA + 1-oleoyl-2-heptadecanoyl-sn-glycerol 3-phosphate
-
-
-
?
heptadecanoyl-CoA + 1-oleoyl-sn-glycerol 3-phosphate
CoA + 1-oleoyl-2-heptadecanoyl-sn-glycerol 3-phosphate
about half of the rate with oleoyl-CoA
-
-
?
linoleoyl-CoA + 1-oleoyl-sn-glycerol 3-phosphate
CoA + 1-oleoyl-2-linoleoyl-sn-glycerol 3-phosphate
-
-
-
?
linoleoyl-CoA + 1-oleoyl-sn-glycerol 3-phosphate
CoA + 1-oleoyl-2-linoleoyl-sn-glycerol 3-phosphate
about half of the rate with oleoyl-CoA
-
-
?
linoleoyl-CoA + 1-oleoyl-sn-glycerol 3-phosphate
CoA + 1-oleoyl-2-linoleoyl-sn-glycerol 3-phosphate
linoleoyl-CoA is second best acyl-CoA substrate
-
-
?
oleoyl-CoA + 1-oleoyl-2-lysophosphatidylinositol
CoA + 1,2-dioleoyl-sn-phosphatidylinositol
-
-
-
-
?
oleoyl-CoA + 1-oleoyl-2-lysophosphatidylinositol
CoA + 1,2-dioleoyl-sn-phosphatidylinositol
-
about 10% of the activity with 1-oleoyl-2-lysophopshatidic acid by AGPAT10/GPAT3
-
-
?
oleoyl-CoA + 1-oleoyl-sn-glycerol 3-phosphate
CoA + 1,2-dioleoyl-sn-glycerol 3-phosphate
-
oleoyl-CoA and 1-oleoyl-sn-glycerol 3-phosphate are the preferred substrates of AGPAT10/GPAT3
-
-
?
oleoyl-CoA + 1-oleoyl-sn-glycerol 3-phosphate
CoA + 1,2-dioleoyl-sn-glycerol 3-phosphate
both substrates are preferred
-
-
?
oleoyl-CoA + 1-oleoyl-sn-glycerol 3-phosphate
CoA + 1,2-dioleoyl-sn-glycerol 3-phosphate
both substrates are preferred
-
-
?
oleoyl-CoA + 1-oleoyl-sn-glycerol 3-phosphate
CoA + 1,2-dioleoyl-sn-glycerol 3-phosphate
both substrates are preferred
-
-
?
oleoyl-CoA + 1-oleoyl-sn-glycerol-3-phosphate
CoA + 1,2-dioleoyl-sn-glycerol 3-phosphate
-
-
-
-
?
oleoyl-CoA + 1-oleoyl-sn-glycerol-3-phosphate
CoA + 1,2-dioleoyl-sn-glycerol 3-phosphate
-
substrate preference higher for oleoyl-CoA than for palmitoyl-CoA and stearoyl-CoA
-
-
?
palmitoyl-CoA + 1-acyl-sn-glycerol 3-phosphate
CoA + 1-acyl-2-palmitoyl-sn-glycerol 3-phosphate
-
-
-
-
?
palmitoyl-CoA + 1-acyl-sn-glycerol 3-phosphate
CoA + 1-acyl-2-palmitoyl-sn-glycerol 3-phosphate
-
-
?
palmitoyl-CoA + 1-acyl-sn-glycerol 3-phosphate
CoA + 1-acyl-2-palmitoyl-sn-glycerol 3-phosphate
acyltransferase motifs I-IV analyzed by sidechain modification, substrate accessibility to the catalytic domain analyzed by competition assay
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-
?
palmitoyl-CoA + 1-oleoyl-sn-glycerol 3-phosphate
CoA + 1-oleoyl-2-palmitoyl-sn-glycerol 3-phosphate
-
-
-
?
palmitoyl-CoA + 1-oleoyl-sn-glycerol 3-phosphate
CoA + 1-oleoyl-2-palmitoyl-sn-glycerol 3-phosphate
-
about 25% of the activity with oleoyl-CoA by AGPAT10/GPAT3
-
-
?
palmitoyl-CoA + 1-oleoyl-sn-glycerol 3-phosphate
CoA + 1-oleoyl-2-palmitoyl-sn-glycerol 3-phosphate
about 40% of the rate with oleoyl-CoA
-
-
?
pentadecanoyl-CoA + 1-oleoyl-sn-glycerol 3-phosphate
CoA + 1-oleoyl-2-pentadecanoyl-sn-glycerol 3-phosphate
50% of the rate with oleoyl-CoA and linoleoyl-CoA
-
-
?
pentadecanoyl-CoA + 1-oleoyl-sn-glycerol 3-phosphate
CoA + 1-oleoyl-2-pentadecanoyl-sn-glycerol 3-phosphate
rate is similar to oleoyl-CoA and linoleoyl-CoA
-
-
?
stearoyl-CoA + 1-oleoyl-sn-glycerol 3-phosphate
CoA + 1-oleoyl-2-stearoyl-sn-glycerol 3-phosphate
-
about 25% of the activity with oleoyl-CoA by AGPAT10/GPAT3
-
-
?
stearoyl-CoA + 1-oleoyl-sn-glycerol 3-phosphate
CoA + 1-oleoyl-2-stearoyl-sn-glycerol 3-phosphate
about 40% of the rate with oleoyl-CoA
-
-
?
additional information
?
-
substrate specificity, overview
-
-
-
additional information
?
-
substrate specificity, overview
-
-
-
additional information
?
-
substrate specificity, overview
-
-
-
additional information
?
-
substrate specificity, overview
-
-
-
additional information
?
-
substrate specificity, overview
-
-
-
additional information
?
-
the enzyme has affinity for fatty acids of acyl chain lengths from 12 to 18 carbons with a slight dependence on the degree of saturation of the fatty acid. However the enzyme does not incorporate long chain fatty acids like C20:0 and C24:0 unless they are saturated
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?
additional information
?
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-
the enzyme has affinity for fatty acids of acyl chain lengths from 12 to 18 carbons with a slight dependence on the degree of saturation of the fatty acid. However the enzyme does not incorporate long chain fatty acids like C20:0 and C24:0 unless they are saturated
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?
additional information
?
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-
AGPAT8 shows moderate acyltransferase activity with oleoyl-CoA but lacks acyl-CoA:lysocardiolipin acyltransferase activity, human AGPAT2, acylation at the sn-2 position with wild-type AGPAT8 is similar for the LPA species containing oleoyl, linoleoyl, linolenoyl, and palmitoyl fatty acids at the sn-1 position, LPA species containing myristoyl, arachidoyl, arachidonoyl are not preferred, substrate specificity in vivo, overview
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-
?
additional information
?
-
-
sn-1-acyl-lysophosphatidic acid and acly-CoA specficity, AGPAT8 is unable to use arachidonoyl-CoA as the acyl donor, overview
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-
?
additional information
?
-
-
CGI-58 is a CoA-dependent lysophosphatidic acid acyltransferase that channels fatty acids released from the hydrolysis of stored triacylglycerols into phospholipids, overview
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?
additional information
?
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LPAAT3 regulates Golgi membrane tubule formation, trafficking, and structure by altering phospholipids and lysophospholipids. LPAAT3 alters ERGIC-53 distribution, a p58 receptor which is a lectin receptor that traffics between the cis-Golgi and the endoplasmic reticulum
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?
additional information
?
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substrate specificity of AGPAT10/GPAT3, overview
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-
?
additional information
?
-
-
the CGI-58 carboxyl terminus includes a highly conserved consensus sequence, HXXXXD, required for acyltransferase activity
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?
additional information
?
-
isoform AGPAT11 shows broad preferences for the lysophosphatidic acid containing saturated fatty acids C16:0-C18:0, including lysophosphatidic acid containing oleic acid. Lysophosphatidic acid with fatty acid C20:4 is acylated at only about one-half maximal rate compared with others. The preferred acyl donor follows the decreasing order of C18:1,C16:0, C18:2, C17:0. Fatty acyl-CoA consisting of short-chain fatty acids C8:0 to C13:0 and very long-chain from C20:0 to C26:0 are not substrates. Enzyme does not display glycerol-3-phosphate acyltransferase activity
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?
additional information
?
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isoform AGPAT11 shows broad preferences for the lysophosphatidic acid containing saturated fatty acids C16:0-C18:0, including lysophosphatidic acid containing oleic acid. Lysophosphatidic acid with fatty acid C20:4 is acylated at only about one-half maximal rate compared with others. The preferred acyl donor follows the decreasing order of C18:1,C16:0, C18:2, C17:0. Fatty acyl-CoA consisting of short-chain fatty acids C8:0 to C13:0 and very long-chain from C20:0 to C26:0 are not substrates. Enzyme does not display glycerol-3-phosphate acyltransferase activity
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?
additional information
?
-
isoform AGPAT3 shows broad preference for lysophosphatidic acids containing saturated or unsaturated fatty acids C16:0-C20:4 and significant esterification of lysophosphatidylinositol in the presence of oleoyl-CoA
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-
?
additional information
?
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isoform AGPAT3 shows broad preference for lysophosphatidic acids containing saturated or unsaturated fatty acids C16:0-C20:4 and significant esterification of lysophosphatidylinositol in the presence of oleoyl-CoA
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?
additional information
?
-
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isoform AGPAT3 shows broad preference for lysophosphatidic acids containing saturated or unsaturated fatty acids C16:0-C20:4 and significant esterification of lysophosphatidylinositol in the presence of oleoyl-CoA
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?
additional information
?
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isoform AGPAT5 demonstrates significant acyltransferase activity toward lysophosphatidylethanolamine in the presence of oleoyl-CoA
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-
?
additional information
?
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isoform AGPAT5 demonstrates significant acyltransferase activity toward lysophosphatidylethanolamine in the presence of oleoyl-CoA
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-
?
additional information
?
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-
isoform AGPAT5 demonstrates significant acyltransferase activity toward lysophosphatidylethanolamine in the presence of oleoyl-CoA
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?
additional information
?
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no substrates: acyl-CoA with fatty acids shorter than C14:0 or longer than C20:0, whether saturated or unsaturated
-
-
?
additional information
?
-
no substrates: acyl-CoA with fatty acids shorter than C14:0 or longer than C20:0, whether saturated or unsaturated
-
-
?
additional information
?
-
-
no substrates: acyl-CoA with fatty acids shorter than C14:0 or longer than C20:0, whether saturated or unsaturated
-
-
?
additional information
?
-
no substrates: acyl-CoA with fatty acids shorter than C14:0 or longer than C20:0, whether saturated or unsaturated. Isoform AGPAT2 is rather restrictive in using 1-oleoyl-sn-glycerol 3-phosphate as acceptor substrate
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-
?
additional information
?
-
no substrates: acyl-CoA with fatty acids shorter than C14:0 or longer than C20:0, whether saturated or unsaturated. Isoform AGPAT2 is rather restrictive in using 1-oleoyl-sn-glycerol 3-phosphate as acceptor substrate
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-
?
additional information
?
-
-
no substrates: acyl-CoA with fatty acids shorter than C14:0 or longer than C20:0, whether saturated or unsaturated. Isoform AGPAT2 is rather restrictive in using 1-oleoyl-sn-glycerol 3-phosphate as acceptor substrate
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?
additional information
?
-
isozymes AGPAT3 and AGPAT5 have weak LPAAT activity compared to isozyme AGPAT2 and utilize other lysophospholipids as substrates
-
-
-
additional information
?
-
isozymes AGPAT3 and AGPAT5 have weak LPAAT activity compared to isozyme AGPAT2 and utilize other lysophospholipids as substrates
-
-
-
additional information
?
-
isozymes AGPAT3 and AGPAT5 have weak LPAAT activity compared to isozyme AGPAT2 and utilize other lysophospholipids as substrates
-
-
-
additional information
?
-
isozymes AGPAT3 and AGPAT5 have weak LPAAT activity compared to isozyme AGPAT2 and utilize other lysophospholipids as substrates
-
-
-
additional information
?
-
isozymes AGPAT3 and AGPAT5 have weak LPAAT activity compared to isozyme AGPAT2 and utilize other lysophospholipids as substrates
-
-
-
additional information
?
-
in vitro, the LPAAT activity of AGPAT1 has a broad specificity for acyl-CoAs, but also has ATP-independent acyl-CoA biosynthetic activity and CoA-dependent transacylation activity. Substrate specificity, overview
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-
-
additional information
?
-
in vitro, the LPAAT activity of AGPAT1 has a broad specificity for acyl-CoAs, but also has ATP-independent acyl-CoA biosynthetic activity and CoA-dependent transacylation activity. Substrate specificity, overview
-
-
-
additional information
?
-
in vitro, the LPAAT activity of AGPAT1 has a broad specificity for acyl-CoAs, but also has ATP-independent acyl-CoA biosynthetic activity and CoA-dependent transacylation activity. Substrate specificity, overview
-
-
-
additional information
?
-
in vitro, the LPAAT activity of AGPAT1 has a broad specificity for acyl-CoAs, but also has ATP-independent acyl-CoA biosynthetic activity and CoA-dependent transacylation activity. Substrate specificity, overview
-
-
-
additional information
?
-
in vitro, the LPAAT activity of AGPAT1 has a broad specificity for acyl-CoAs, but also has ATP-independent acyl-CoA biosynthetic activity and CoA-dependent transacylation activity. Substrate specificity, overview
-
-
-
additional information
?
-
substrate specificity, overview. Besides lysophosphatidic acid, the isozyme also utilizes lyso-phosphocholine, -phosphoethanolamine and -phosphatidylserine as acyl acceptors. AGPAT3, AGPAT4, and AGPAT5 have LPAAT activity with oleoyl-CoA as the acyl donor, but also have LPLAT activity with a preference for polyunsaturated acyl-CoAs
-
-
-
additional information
?
-
substrate specificity, overview. Besides lysophosphatidic acid, the isozyme also utilizes lyso-phosphocholine, -phosphoethanolamine and -phosphatidylserine as acyl acceptors. AGPAT3, AGPAT4, and AGPAT5 have LPAAT activity with oleoyl-CoA as the acyl donor, but also have LPLAT activity with a preference for polyunsaturated acyl-CoAs
-
-
-
additional information
?
-
substrate specificity, overview. Besides lysophosphatidic acid, the isozyme also utilizes lyso-phosphocholine, -phosphoethanolamine and -phosphatidylserine as acyl acceptors. AGPAT3, AGPAT4, and AGPAT5 have LPAAT activity with oleoyl-CoA as the acyl donor, but also have LPLAT activity with a preference for polyunsaturated acyl-CoAs
-
-
-
additional information
?
-
substrate specificity, overview. Besides lysophosphatidic acid, the isozyme also utilizes lyso-phosphocholine, -phosphoethanolamine and -phosphatidylserine as acyl acceptors. AGPAT3, AGPAT4, and AGPAT5 have LPAAT activity with oleoyl-CoA as the acyl donor, but also have LPLAT activity with a preference for polyunsaturated acyl-CoAs
-
-
-
additional information
?
-
substrate specificity, overview. Besides lysophosphatidic acid, the isozyme also utilizes lyso-phosphocholine, -phosphoethanolamine and -phosphatidylserine as acyl acceptors. AGPAT3, AGPAT4, and AGPAT5 have LPAAT activity with oleoyl-CoA as the acyl donor, but also have LPLAT activity with a preference for polyunsaturated acyl-CoAs
-
-
-
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1-acylglycerol-3-phosphate o-acyltransferase deficiency
ABHD5 blunts the sensitivity of colorectal cancer to fluorouracil via promoting autophagic uracil yield.
1-acylglycerol-3-phosphate o-acyltransferase deficiency
ABHD5 interacts with BECN1 to regulate autophagy and tumorigenesis of colon cancer independent of PNPLA2.
1-acylglycerol-3-phosphate o-acyltransferase deficiency
Absence of AGPAT2 impairs brown adipogenesis, increases IFN stimulated gene expression and alters mitochondrial morphology.
1-acylglycerol-3-phosphate o-acyltransferase deficiency
AGPAT2 deficiency impairs adipogenic differentiation in primary cultured preadipocytes in a non-autophagy or apoptosis dependent mechanism.
1-acylglycerol-3-phosphate o-acyltransferase deficiency
Cancer-derived exosomal TRIM59 regulates macrophage NLRP3 inflammasome activation to promote lung cancer progression.
1-acylglycerol-3-phosphate o-acyltransferase deficiency
Inherited lipodystrophies and hypertriglyceridemia.
1-acylglycerol-3-phosphate o-acyltransferase deficiency
Loss of abhd5 promotes colorectal tumor development and progression by inducing aerobic glycolysis and epithelial-mesenchymal transition.
1-acylglycerol-3-phosphate o-acyltransferase deficiency
Macrophage ABHD5 suppresses NF-?B-dependent matrix metalloproteinase expression and cancer metastasis.
1-acylglycerol-3-phosphate o-acyltransferase deficiency
Molecular mechanisms of hepatic steatosis and insulin resistance in the AGPAT2-deficient mouse model of congenital generalized lipodystrophy.
1-acylglycerol-3-phosphate o-acyltransferase deficiency
Pathology of Congenital Generalized Lipodystrophy in Agpat2 -/-Mice.
1-acylglycerol-3-phosphate o-acyltransferase deficiency
Truncation of CGI-58 protein causes malformation of lamellar granules resulting in ichthyosis in Dorfman-Chanarin syndrome.
Adenomatous Polyps
Loss of abhd5 promotes colorectal tumor development and progression by inducing aerobic glycolysis and epithelial-mesenchymal transition.
Carcinogenesis
ABHD5 interacts with BECN1 to regulate autophagy and tumorigenesis of colon cancer independent of PNPLA2.
Carcinogenesis
Loss of abhd5 promotes colorectal tumor development and progression by inducing aerobic glycolysis and epithelial-mesenchymal transition.
Carcinoma
Expression of lysophosphatidic acid acyltransferase beta (LPAAT-beta) in ovarian carcinoma: correlation with tumour grading and prognosis.
Carcinoma
Interaction of lipopolysaccharide with a mammalian lyso-phosphatidate acyltransferase (LPAAT) transfected into E. coli, and effect of lisofylline on LPAAT transfected into mammalian cells.
Carcinoma
Lipid synthesis and processing proteins ABHD5, PGRMC1 and squalene synthase can serve as novel immunohistochemical markers for sebaceous neoplasms and differentiate sebaceous carcinoma from sebaceoma and basal cell carcinoma with clear cell features.
Carcinoma
Lysophosphatidic acid acyltransferase-beta (LPAAT-beta) is highly expressed in advanced ovarian cancer and is associated with aggressive histology and poor survival.
Carcinoma, Basal Cell
Lipid synthesis and processing proteins ABHD5, PGRMC1 and squalene synthase can serve as novel immunohistochemical markers for sebaceous neoplasms and differentiate sebaceous carcinoma from sebaceoma and basal cell carcinoma with clear cell features.
Cardiomyopathies
Inborn errors of cytoplasmic triglyceride metabolism.
Cardiovascular Diseases
Leu124Serfs*26, a novel AGPAT2 mutation in congenital generalized lipodystrophy with early cardiovascular complications.
carnitine o-palmitoyltransferase deficiency
High frequency of ETFDH c.250G>A mutation in Taiwanese patients with late-onset lipid storage myopathy.
Colonic Neoplasms
ABHD5 interacts with BECN1 to regulate autophagy and tumorigenesis of colon cancer independent of PNPLA2.
Colonic Neoplasms
ColoLipidGene: signature of lipid metabolism-related genes to predict prognosis in stage-II colon cancer patients.
Colonic Neoplasms
Loss of abhd5 promotes colorectal tumor development and progression by inducing aerobic glycolysis and epithelial-mesenchymal transition.
Colorectal Neoplasms
ABHD5 blunts the sensitivity of colorectal cancer to fluorouracil via promoting autophagic uracil yield.
Colorectal Neoplasms
ABHD5 interacts with BECN1 to regulate autophagy and tumorigenesis of colon cancer independent of PNPLA2.
Colorectal Neoplasms
Enzymatic activity of the human 1-acylglycerol-3-phosphate-O-acyltransferase isoform 11 (AGPAT11): upregulated in breast and cervical cancers.
Colorectal Neoplasms
Loss of abhd5 promotes colorectal tumor development and progression by inducing aerobic glycolysis and epithelial-mesenchymal transition.
Colorectal Neoplasms
Loss of Abhd5 Promotes Colorectal Tumor Development and Progression by Inducing Aerobic Glycolysis and Epithelial-Mesenchymal Transition.
Colorectal Neoplasms
Macrophage ABHD5 promotes colorectal cancer growth by suppressing spermidine production by SRM.
Colorectal Neoplasms
Macrophage ABHD5 suppresses NF-?B-dependent matrix metalloproteinase expression and cancer metastasis.
Coronary Artery Disease
Genome-Wide Association Study Identifies Novel Loci Associated with Circulating Phospho- and Sphingolipid Concentrations.
Dermatitis, Exfoliative
Chanarin Dorfman syndrome: a case report with novel nonsense mutation.
Dermatitis, Exfoliative
Early onset of Chanarin-Dorfman syndrome with severe liver involvement in a patient with a complex rearrangement of ABHD5 promoter.
Diabetes Mellitus
Leptin ameliorates insulin resistance and hepatic steatosis in Agpat2-/- lipodystrophic mice independent of hepatocyte leptin receptors.
Diabetes Mellitus, Type 2
Genome-Wide Association Study Identifies Novel Loci Associated with Circulating Phospho- and Sphingolipid Concentrations.
Diabetes, Gestational
Downregulated ABHD5 Aggravates Insulin Resistance of Trophoblast Cells During Gestational Diabetes Mellitus.
Dyslipidemias
Inherited non-alcoholic fatty liver disease and dyslipidemia due to monoallelic ABHD5 mutations.
Embryo Loss
Plastid lysophosphatidyl acyltransferase is essential for embryo development in Arabidopsis.
Endometrial Neoplasms
Lysophosphatidic acid acyltransferase-beta is a prognostic marker and therapeutic target in gynecologic malignancies.
Endometrial Neoplasms
Oncogenic role of ABHD5 in endometrial cancer.
Exfoliation Syndrome
Molecular Genetics of Glaucoma: Subtype and Ethnicity Considerations.
Exfoliation Syndrome
NEW GENETIC MARKERS ASSOCIATED WITH SUSCEPTIBILITY TO EXFOLIATION SYNDROME AMONG GEORGIAN POPULATION.
Fatty Liver
Dynamic interactions of ABHD5 with PNPLA3 regulate triacylglycerol metabolism in brown adipocytes.
Fatty Liver
Early onset of Chanarin-Dorfman syndrome with severe liver involvement in a patient with a complex rearrangement of ABHD5 promoter.
Fatty Liver
Inherited non-alcoholic fatty liver disease and dyslipidemia due to monoallelic ABHD5 mutations.
Fatty Liver
Steatohepatitis and unsuspected micronodular cirrhosis in Dorfman-Chanarin syndrome with documented ABHD5 mutation.
Fatty Liver
Two cases of non-alcoholic fatty liver disease caused by biallelic ABHD5 mutations.
Genetic Diseases, Inborn
Genetics of Exfoliation Syndrome.
Genetic Diseases, Inborn
Neutral lipid storage disease: genetic disorders caused by mutations in adipose triglyceride lipase/PNPLA2 or CGI-58/ABHD5.
Glucose Metabolism Disorders
Downregulated ABHD5 Aggravates Insulin Resistance of Trophoblast Cells During Gestational Diabetes Mellitus.
Heart Failure
The lipid droplet-associated protein ABHD5 protects the heart through proteolysis of HDAC4.
Hematologic Neoplasms
[Relationship between Lysophosphatide Acid Acyltransferase beta and Tumor - Review.]
Hepatitis C
The ATGL lipase cooperates with ABHD5 to mobilize lipids for hepatitis C virus assembly.
Hepatomegaly
Early onset of Chanarin-Dorfman syndrome with severe liver involvement in a patient with a complex rearrangement of ABHD5 promoter.
Hepatomegaly
The gene encoding adipose triglyceride lipase (PNPLA2) is mutated in neutral lipid storage disease with myopathy.
Hyperlipidemias
A novel mutation of ABHD5 gene in a Chanarin Dorfman patient with unusual dermatological findings.
Hypertriglyceridemia
Inborn errors of cytoplasmic triglyceride metabolism.
Ichthyosiform Erythroderma, Congenital
Early onset of Chanarin-Dorfman syndrome with severe liver involvement in a patient with a complex rearrangement of ABHD5 promoter.
Ichthyosis
ABHD5 stimulates PNPLA1-mediated ?-O-acylceramide biosynthesis essential for a functional skin permeability barrier.
Ichthyosis
Clinical and genetic analysis of lipid storage myopathies.
Ichthyosis
High frequency of ETFDH c.250G>A mutation in Taiwanese patients with late-onset lipid storage myopathy.
Ichthyosis
Inborn errors of cytoplasmic triglyceride metabolism.
Ichthyosis
Molecular mechanism of the ichthyosis pathology of Chanarin-Dorfman syndrome: Stimulation of PNPLA1-catalyzed ?-O-acylceramide production by ABHD5.
Ichthyosis
Recurrent N209* ABHD5 mutation in two unreported families with Chanarin Dorfman Syndrome.
Ichthyosis
Steatohepatitis and unsuspected micronodular cirrhosis in Dorfman-Chanarin syndrome with documented ABHD5 mutation.
Ichthyosis
The gene encoding adipose triglyceride lipase (PNPLA2) is mutated in neutral lipid storage disease with myopathy.
Ichthyosis
Truncation of CGI-58 protein causes malformation of lamellar granules resulting in ichthyosis in Dorfman-Chanarin syndrome.
Ichthyosis
[Neutral lipid storage diseases and ATGL (adipose triglyceride lipase) and CGI-58/ABHD5 (alpha-beta hydrolase domain-containing 5) deficiency: myopathy, ichthyosis, but no obesity]
Infections
Dengue virus reduces AGPAT1 expression to alter phospholipids and enhance infection in Aedes aegypti.
Insulin Resistance
AGPAT2 deficiency impairs adipogenic differentiation in primary cultured preadipocytes in a non-autophagy or apoptosis dependent mechanism.
Insulin Resistance
AGPAT2 gene mutation in a child with Berardinelli-Seip congenital lipodystrophy syndrome.
Insulin Resistance
Alterations in Lipid Signaling Underlie Lipodystrophy Secondary to AGPAT2 Mutations.
Insulin Resistance
Diseases of adipose tissue: genetic and acquired lipodystrophies.
Insulin Resistance
Downregulated ABHD5 Aggravates Insulin Resistance of Trophoblast Cells During Gestational Diabetes Mellitus.
Insulin Resistance
Hepatic gluconeogenesis is enhanced by phosphatidic acid which remains uninhibited by insulin in lipodystrophic Agpat2-/- mice.
Insulin Resistance
How to diagnose a lipodystrophy syndrome.
Insulin Resistance
Human AGPAT isoforms 1 and 2: Biochemical characterization and their inability to rescue hepatic steatosis in Agpat2-/- lipodystrophic mice.
Insulin Resistance
Leptin ameliorates insulin resistance and hepatic steatosis in Agpat2-/- lipodystrophic mice independent of hepatocyte leptin receptors.
Insulin Resistance
Monogenic forms of insulin resistance: apertures that expose the common metabolic syndrome.
Insulin Resistance
[Monogenic severe insulin resistance syndromes]
Intellectual Disability
Dorfman-Chanarin syndrome without mental retardation caused by a homozygous ABHD5 splice site mutation that skips exon 6.
Intellectual Disability
Mutations in Gng3lg and AGPAT2 in Berardinelli-Seip congenital lipodystrophy and Brunzell syndrome: phenotype variability suggests important modifier effects.
Leukemia
Antileukemic activity of lysophosphatidic acid acyltransferase-beta inhibitor CT32228 in chronic myelogenous leukemia sensitive and resistant to imatinib.
Leukemia
Effect of lysophosphatidic acid acyltransferase-beta inhibition in acute leukemia.
Leukemia
[Lysophosphatidic acid acyltransferase ? gene expression in newly diagnosed leukemia patients].
Leukemia, Myelogenous, Chronic, BCR-ABL Positive
Antileukemic activity of lysophosphatidic acid acyltransferase-beta inhibitor CT32228 in chronic myelogenous leukemia sensitive and resistant to imatinib.
Leukemia, Myelogenous, Chronic, BCR-ABL Positive
[Lysophosphatidic acid acyltransferase ? gene expression in newly diagnosed leukemia patients].
Leukemia, Myeloid, Acute
[Lysophosphatidic acid acyltransferase ? gene expression in newly diagnosed leukemia patients].
Leukemia, Promyelocytic, Acute
[Lysophosphatidic acid acyltransferase ? gene expression in newly diagnosed leukemia patients].
Lipodystrophy
A Frame-Shift Mutation in CAV1 Is Associated with a Severe Neonatal Progeroid and Lipodystrophy Syndrome.
Lipodystrophy
A regulatory role for 1-acylglycerol-3-phosphate-O-acyltransferase 2 in adipocyte differentiation.
Lipodystrophy
A Single Complex Agpat2 Allele in a Patient With Partial Lipodystrophy.
Lipodystrophy
AGPAT2 deficiency impairs adipogenic differentiation in primary cultured preadipocytes in a non-autophagy or apoptosis dependent mechanism.
Lipodystrophy
AGPAT2 gene mutation in a child with Berardinelli-Seip congenital lipodystrophy syndrome.
Lipodystrophy
AGPAT2 is essential for postnatal development and maintenance of white and brown adipose tissue.
Lipodystrophy
Alterations in Lipid Signaling Underlie Lipodystrophy Secondary to AGPAT2 Mutations.
Lipodystrophy
Case report: Dental management of Berardinelli-Seip congenital lipodystrophy.
Lipodystrophy
Congenital generalized lipodystrophy: significance of triglyceride biosynthetic pathways.
Lipodystrophy
Discovering metabolic disease gene interactions by correlated effects on cellular morphology.
Lipodystrophy
Early infantile cardiomyopathy and liver disease: a multisystemic disorder caused by congenital lipodystrophy.
Lipodystrophy
Efficacy of leptin therapy in the different forms of human lipodystrophy.
Lipodystrophy
Erratum to: Identification and Characterisation of a Novel Pathogenic Mutation in the Human Lipodystrophy Gene AGPAT2 : C48R: A Novel Mutation in AGPAT2.
Lipodystrophy
Exploring the pathophysiology behind the more common genetic and acquired lipodystrophies.
Lipodystrophy
Genetic basis of congenital generalized lipodystrophy.
Lipodystrophy
Genetic disorders of adipose tissue development, differentiation, and death.
Lipodystrophy
Higher adiponectin levels in patients with Berardinelli-Seip congenital lipodystrophy due to seipin as compared with 1-acylglycerol-3-phosphate-o-acyltransferase-2 deficiency.
Lipodystrophy
Identification and Characterisation of a Novel Pathogenic Mutation in the Human Lipodystrophy Gene AGPAT2 : C48R: A Novel Mutation in AGPAT2.
Lipodystrophy
Inherited lipodystrophies and hypertriglyceridemia.
Lipodystrophy
Lipodystrophies: Disorders of adipose tissue biology.
Lipodystrophy
Monogenic forms of insulin resistance: apertures that expose the common metabolic syndrome.
Lipodystrophy
Mutations in Gng3lg and AGPAT2 in Berardinelli-Seip congenital lipodystrophy and Brunzell syndrome: phenotype variability suggests important modifier effects.
Lipodystrophy
Mutations in the seipin and AGPAT2 genes clustering in consanguineous families with Berardinelli-Seip congenital lipodystrophy from two separate geographical regions of Brazil.
Lipodystrophy
Novel BSCL2 gene mutation E189X in Chinese congenital generalized lipodystrophy child with early onset diabetes mellitus.
Lipodystrophy
Oligomers of the lipodystrophy protein seipin may co-ordinate GPAT3 and AGPAT2 enzymes to facilitate adipocyte differentiation.
Lipodystrophy
Pathology of Congenital Generalized Lipodystrophy in Agpat2 -/-Mice.
Lipodystrophy
Phenotypic and genetic heterogeneity in congenital generalized lipodystrophy.
Lipodystrophy
Phenotypic heterogeneity in biochemical parameters correlates with mutations in AGPAT2 or Seipin genes among Berardinelli-Seip congenital lipodystrophy patients.
Lipodystrophy
Prevalence of mutations in AGPAT2 among human lipodystrophies.
Lipodystrophy, Congenital Generalized
A novel AGPAT2 mutation associated with a case of late-diagnosed congenital generalized lipodystrophy type 1.
Lipodystrophy, Congenital Generalized
A Patient with Congenital Generalized Lipodystrophy Due To a Novel Mutation in BSCL2: Indications for Secondary Mitochondrial Dysfunction.
Lipodystrophy, Congenital Generalized
A rare frameshift mutation in the AGPAT2 gene in a family from gaza with congenital generalized lipodystrophy.
Lipodystrophy, Congenital Generalized
A regulatory role for 1-acylglycerol-3-phosphate-O-acyltransferase 2 in adipocyte differentiation.
Lipodystrophy, Congenital Generalized
A Single Complex Agpat2 Allele in a Patient With Partial Lipodystrophy.
Lipodystrophy, Congenital Generalized
Absence of AGPAT2 impairs brown adipogenesis, increases IFN stimulated gene expression and alters mitochondrial morphology.
Lipodystrophy, Congenital Generalized
AGPAT2 gene mutation in a child with Berardinelli-Seip congenital lipodystrophy syndrome.
Lipodystrophy, Congenital Generalized
AGPAT2 is mutated in congenital generalized lipodystrophy linked to chromosome 9q34.
Lipodystrophy, Congenital Generalized
Alterations in Lipid Signaling Underlie Lipodystrophy Secondary to AGPAT2 Mutations.
Lipodystrophy, Congenital Generalized
Berardinelli-Seip syndrome patient with novel AGPAT2 splicesite mutation and concomitant development of non-diabetic polyneuropathy
Lipodystrophy, Congenital Generalized
Case report: Dental management of Berardinelli-Seip congenital lipodystrophy.
Lipodystrophy, Congenital Generalized
Description of an AGPAT2 pathologic allelic variant in a 54-year-old Caucasian woman with Berardinelli-Seip syndrome.
Lipodystrophy, Congenital Generalized
Diseases of adipose tissue: genetic and acquired lipodystrophies.
Lipodystrophy, Congenital Generalized
Divergent metabolic phenotype between two sisters with congenital generalized lipodystrophy due to double AGPAT2 homozygous mutations. a clinical, genetic and in silico study.
Lipodystrophy, Congenital Generalized
Enzymatic activity of naturally occurring 1-acylglycerol-3-phosphate-O-acyltransferase 2 mutants associated with congenital generalized lipodystrophy.
Lipodystrophy, Congenital Generalized
Exploring the pathophysiology behind the more common genetic and acquired lipodystrophies.
Lipodystrophy, Congenital Generalized
Expression of AGPAT2, an enzyme involved in the glycerophospholipid/triacylglycerol biosynthesis pathway, is directly regulated by HIF-1 and promotes survival and etoposide resistance of cancer cells under hypoxia.
Lipodystrophy, Congenital Generalized
Further delineation of AGPAT2 and BSCL2 related congenital generalized lipodystrophy in young infants.
Lipodystrophy, Congenital Generalized
Genetic basis of congenital generalized lipodystrophy.
Lipodystrophy, Congenital Generalized
Identification of a novel nonsense mutation and a missense substitution in the AGPAT2 gene causing congenital generalized lipodystrophy type 1.
Lipodystrophy, Congenital Generalized
Inherited lipodystrophies and hypertriglyceridemia.
Lipodystrophy, Congenital Generalized
Leptin ameliorates insulin resistance and hepatic steatosis in Agpat2-/- lipodystrophic mice independent of hepatocyte leptin receptors.
Lipodystrophy, Congenital Generalized
Leu124Serfs*26, a novel AGPAT2 mutation in congenital generalized lipodystrophy with early cardiovascular complications.
Lipodystrophy, Congenital Generalized
Lipodystrophies: Disorders of adipose tissue biology.
Lipodystrophy, Congenital Generalized
Lipodystrophies: Genetic and Acquired Body Fat Disorders.
Lipodystrophy, Congenital Generalized
Metabolic, Reproductive, and Neurologic Abnormalities in Agpat1-Null Mice.
Lipodystrophy, Congenital Generalized
Molecular mechanisms of hepatic steatosis and insulin resistance in the AGPAT2-deficient mouse model of congenital generalized lipodystrophy.
Lipodystrophy, Congenital Generalized
Monogenic forms of insulin resistance: apertures that expose the common metabolic syndrome.
Lipodystrophy, Congenital Generalized
Mutations in Gng3lg and AGPAT2 in Berardinelli-Seip congenital lipodystrophy and Brunzell syndrome: phenotype variability suggests important modifier effects.
Lipodystrophy, Congenital Generalized
Mutations in the seipin and AGPAT2 genes clustering in consanguineous families with Berardinelli-Seip congenital lipodystrophy from two separate geographical regions of Brazil.
Lipodystrophy, Congenital Generalized
Novel BSCL2 gene mutation E189X in Chinese congenital generalized lipodystrophy child with early onset diabetes mellitus.
Lipodystrophy, Congenital Generalized
Novel mutations of the BSCL2 and AGPAT2 genes in ten families with Berardinelli-Seip congenital generalized lipodystrophy syndrome.
Lipodystrophy, Congenital Generalized
Oil Red-O Positive lipid blobs on peripheral blood film examination in a muscular infant with the diagnosis of Berardinelli-Seip syndrome.
Lipodystrophy, Congenital Generalized
Pathology of Congenital Generalized Lipodystrophy in Agpat2 -/-Mice.
Lipodystrophy, Congenital Generalized
Phenotypic and genetic heterogeneity in congenital generalized lipodystrophy.
Lipodystrophy, Congenital Generalized
Phenotypic heterogeneity in biochemical parameters correlates with mutations in AGPAT2 or Seipin genes among Berardinelli-Seip congenital lipodystrophy patients.
Lipodystrophy, Congenital Generalized
Phenotypic heterogeneity in body fat distribution in patients with congenital generalized lipodystrophy caused by mutations in the AGPAT2 or seipin genes.
Lipodystrophy, Congenital Generalized
Seipin oligomers can interact directly with AGPAT2 and lipin 1, physically scaffolding critical regulators of adipogenesis.
Lipodystrophy, Congenital Generalized
[Identification of a novel AGPAT2 variant in a Chinese patient with congenital generalized lipodystrophy type 1].
Lipodystrophy, Congenital Generalized
[Primary lipodystrophies]
Lipodystrophy, Familial Partial
Monogenic forms of insulin resistance: apertures that expose the common metabolic syndrome.
Liver Cirrhosis
Liver cirrhosis in an infant with Chanarin-Dorfman syndrome caused by a novel splice-site mutation in ABHD5.
Liver Diseases
Dynamic interactions of ABHD5 with PNPLA3 regulate triacylglycerol metabolism in brown adipocytes.
Liver Diseases
Inherited non-alcoholic fatty liver disease and dyslipidemia due to monoallelic ABHD5 mutations.
Liver Diseases
Two cases of non-alcoholic fatty liver disease caused by biallelic ABHD5 mutations.
Lung Neoplasms
Cancer-derived exosomal TRIM59 regulates macrophage NLRP3 inflammasome activation to promote lung cancer progression.
Lymphatic Metastasis
Oncogenic role of ABHD5 in endometrial cancer.
Lymphoma
Induction of apoptosis using inhibitors of lysophosphatidic acid acyltransferase-beta and anti-CD20 monoclonal antibodies for treatment of human non-Hodgkin's lymphomas.
Lymphoma, Non-Hodgkin
Induction of apoptosis using inhibitors of lysophosphatidic acid acyltransferase-beta and anti-CD20 monoclonal antibodies for treatment of human non-Hodgkin's lymphomas.
Marfan Syndrome
How to diagnose a lipodystrophy syndrome.
Metabolic Syndrome
Monogenic forms of insulin resistance: apertures that expose the common metabolic syndrome.
Multiple Myeloma
Antitumor activity of lysophosphatidic acid acyltransferase-beta inhibitors, a novel class of agents, in multiple myeloma.
Muscular Diseases
Clinical and genetic analysis of lipid storage myopathies.
Muscular Diseases
High frequency of ETFDH c.250G>A mutation in Taiwanese patients with late-onset lipid storage myopathy.
Muscular Diseases
Inborn errors of cytoplasmic triglyceride metabolism.
Muscular Diseases
The gene encoding adipose triglyceride lipase (PNPLA2) is mutated in neutral lipid storage disease with myopathy.
Muscular Diseases
[Neutral lipid storage diseases and ATGL (adipose triglyceride lipase) and CGI-58/ABHD5 (alpha-beta hydrolase domain-containing 5) deficiency: myopathy, ichthyosis, but no obesity]
Neoplasm Metastasis
Lysophosphatidic acid acyltransferase-beta (LPAAT-beta) is highly expressed in advanced ovarian cancer and is associated with aggressive histology and poor survival.
Neoplasm Metastasis
Macrophage ABHD5 suppresses NF-?B-dependent matrix metalloproteinase expression and cancer metastasis.
Neoplasm Metastasis
Oncogenic role of ABHD5 in endometrial cancer.
Neoplasms
ABHD5 interacts with BECN1 to regulate autophagy and tumorigenesis of colon cancer independent of PNPLA2.
Neoplasms
ABHD5 suppresses cancer cell anabolism through lipolysis-dependent activation of the AMPK/mTORC1 pathway.
Neoplasms
Antileukemic activity of lysophosphatidic acid acyltransferase-beta inhibitor CT32228 in chronic myelogenous leukemia sensitive and resistant to imatinib.
Neoplasms
Cancer-derived exosomal TRIM59 regulates macrophage NLRP3 inflammasome activation to promote lung cancer progression.
Neoplasms
Circular RNA cMras Suppresses the Progression of Lung Adenocarcinoma Through ABHD5/ATGL Axis Using NF-?B Signaling Pathway.
Neoplasms
Cloning and expression of two human lysophosphatidic acid acyltransferase cDNAs that enhance cytokine-induced signaling responses in cells.
Neoplasms
Effect of lysophosphatidic acid acyltransferase-beta inhibition in acute leukemia.
Neoplasms
Enzymatic activity of the human 1-acylglycerol-3-phosphate-O-acyltransferase isoform 11 (AGPAT11): upregulated in breast and cervical cancers.
Neoplasms
Expression of AGPAT2, an enzyme involved in the glycerophospholipid/triacylglycerol biosynthesis pathway, is directly regulated by HIF-1 and promotes survival and etoposide resistance of cancer cells under hypoxia.
Neoplasms
Expression of lysophosphatidic acid acyltransferase beta (LPAAT-beta) in ovarian carcinoma: correlation with tumour grading and prognosis.
Neoplasms
Identification of a Novel Human Lysophosphatidic Acid Acyltransferase, LPAAT-theta, Which Activates mTOR Pathway.
Neoplasms
Inhibition of lysophosphatidic acid acyltransferase beta disrupts proliferative and survival signals in normal cells and induces apoptosis of tumor cells.
Neoplasms
Lipid synthesis and processing proteins ABHD5, PGRMC1 and squalene synthase can serve as novel immunohistochemical markers for sebaceous neoplasms and differentiate sebaceous carcinoma from sebaceoma and basal cell carcinoma with clear cell features.
Neoplasms
Loss of abhd5 promotes colorectal tumor development and progression by inducing aerobic glycolysis and epithelial-mesenchymal transition.
Neoplasms
Loss of ABHD5 promotes the aggressiveness of prostate cancer cells.
Neoplasms
Lysophosphatidic acid acyltransferase ? (LPAAT?) promotes the tumor growth of human osteosarcoma.
Neoplasms
Lysophosphatidic acid acyltransferase-beta (LPAAT-beta) is highly expressed in advanced ovarian cancer and is associated with aggressive histology and poor survival.
Neoplasms
Lysophosphatidic acid acyltransferase-beta is a prognostic marker and therapeutic target in gynecologic malignancies.
Neoplasms
Lysophosphatidic acid acyltransferase-beta: a novel target for induction of tumour cell apoptosis.
Neoplasms
Macrophage ABHD5 suppresses NF-?B-dependent matrix metalloproteinase expression and cancer metastasis.
Neoplasms
Oncogenic role of ABHD5 in endometrial cancer.
Neoplasms
The structure and functions of human lysophosphatidic acid acyltransferases.
Neoplasms
[Relationship between Lysophosphatide Acid Acyltransferase beta and Tumor - Review.]
Non-alcoholic Fatty Liver Disease
A novel mutation of ABHD5 gene in a Chanarin Dorfman patient with unusual dermatological findings.
Non-alcoholic Fatty Liver Disease
Inherited non-alcoholic fatty liver disease and dyslipidemia due to monoallelic ABHD5 mutations.
Non-alcoholic Fatty Liver Disease
Two cases of non-alcoholic fatty liver disease caused by biallelic ABHD5 mutations.
Obesity
Adipose-selective overexpression of ABHD5/CGI-58 does not increase lipolysis or protect against diet-induced obesity.
Obesity
Congenital generalized lipodystrophy: significance of triglyceride biosynthetic pathways.
Obesity
Transcriptomic and epigenetic changes in early liver steatosis associated to obesity: Effect of dietary methyl donor supplementation.
Obesity
[Neutral lipid storage diseases and ATGL (adipose triglyceride lipase) and CGI-58/ABHD5 (alpha-beta hydrolase domain-containing 5) deficiency: myopathy, ichthyosis, but no obesity]
Osteosarcoma
Lysophosphatidic acid acyltransferase ? (LPAAT?) promotes the tumor growth of human osteosarcoma.
Osteosarcoma
MicroRNA-24 inhibits osteosarcoma cell proliferation both in vitro and in vivo by targeting LPAAT?.
Osteosarcoma
Silencing LPAAT? inhibits tumor growth of cisplatin-resistant human osteosarcoma in vivo and in vitro.
Ovarian Neoplasms
Clinical significance of combining salivary mRNAs and carcinoembryonic antigen for ovarian cancer detection.
Ovarian Neoplasms
Expression of lysophosphatidic acid acyltransferase beta (LPAAT-beta) in ovarian carcinoma: correlation with tumour grading and prognosis.
Ovarian Neoplasms
LPAAT-beta identifies aggressive ovarian cancer.
Ovarian Neoplasms
Lysophosphatidic acid acyltransferase-beta is a prognostic marker and therapeutic target in gynecologic malignancies.
Pancreatic Neoplasms
Identification of prognostic lipid droplet-associated genes in pancreatic cancer patients via bioinformatics analysis.
Polyneuropathies
Berardinelli-Seip syndrome patient with novel AGPAT2 splicesite mutation and concomitant development of non-diabetic polyneuropathy
Precursor Cell Lymphoblastic Leukemia-Lymphoma
[Lysophosphatidic acid acyltransferase ? gene expression in newly diagnosed leukemia patients].
Prostatic Neoplasms
ABHD5 suppresses cancer cell anabolism through lipolysis-dependent activation of the AMPK/mTORC1 pathway.
Prostatic Neoplasms
Loss of ABHD5 promotes the aggressiveness of prostate cancer cells.
Prostatic Neoplasms
Positive regulation of prostate cancer cell growth by lipid droplet forming and processing enzymes DGAT1 and ABHD5.
Protein Deficiency
Truncation of CGI-58 protein causes malformation of lamellar granules resulting in ichthyosis in Dorfman-Chanarin syndrome.
Pulmonary Disease, Chronic Obstructive
Gene and metabolite time-course response to cigarette smoking in mouse lung and plasma.
Sepsis
Interaction of lipopolysaccharide with a mammalian lyso-phosphatidate acyltransferase (LPAAT) transfected into E. coli, and effect of lisofylline on LPAAT transfected into mammalian cells.
Thymoma
Inherited lipodystrophies and hypertriglyceridemia.
Thymoma
Lipodystrophies: Disorders of adipose tissue biology.
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Mizuno, M.; Sugiura, Y.; Okuyama, H.
Properties of acyl-coenzyme A:1-acylglycerophosphate acyltransferase and lipases in porcine erythrocyte membranes
J. Lipid Res.
25
843-850
1984
Homo sapiens, Sus scrofa
brenda
Aguado, B.; Campbell, R.D.
Characterization of a human lysophosphatidic acid acyltransferase that is encoded by a gene located in the class III region of the human major histocompatibility complex
J. Biol. Chem.
273
4096-4105
1998
Homo sapiens (Q99943), Homo sapiens
brenda
Haque, W.; Garg, A.; Agarwal, A.K.
Enzymatic activity of naturally occurring 1-acylglycerol-3-phosphate-O-acyltransferase 2 mutants associated with congenital generalized lipodystrophy
Biochem. Biophys. Res. Commun.
327
446-453
2005
Homo sapiens
brenda
Agarwal, A.K.; Barnes, R.I.; Garg, A.
Functional characterization of human 1-acylglycerol-3-phosphate acyltransferase isoform 8: cloning, tissue distribution, gene structure, and enzymatic activity
Arch. Biochem. Biophys.
449
64-76
2006
Homo sapiens, Mus musculus
brenda
Ye, G.M.; Chen, C.; Huang, S.; Han, D.D.; Guo, J.H.; Wan, B.; Yu, L.
Cloning and characterization a novel human 1-acyl-sn-glycerol-3-phosphate acyltransferase gene AGPAT7
DNA Seq.
16
386-390
2005
Homo sapiens (Q643R3), Homo sapiens
brenda
Gale, S.E.; Frolov, A.; Han, X.; Bickel, P.E.; Cao, L.; Bowcock, A.; Schaffer, J.E.; Ory, D.S.
A regulatory role for 1-acylglycerol-3-phosphate-O-acyltransferase 2 in adipocyte differentiation
J. Biol. Chem.
281
11082-11089
2006
Homo sapiens (O15120)
brenda
Yamashita, A.; Nakanishi, H.; Suzuki, H.; Kamata, R.; Tanaka, K.; Waku, K.; Sugiura, T.
Topology of acyltransferase motifs and substrate specificity and accessibility in 1-acyl-sn-glycero-3-phosphate acyltransferase 1
Biochim. Biophys. Acta
1771
1202-1215
2007
Homo sapiens (Q99943), Homo sapiens
brenda
Ghosh, A.K.; Ramakrishnan, G.; Chandramohan, C.; Rajasekharan, R.
CGI-58, the causative gene for Chanarin-Dorfman syndrome, mediates acylation of lysophosphatidic acid
J. Biol. Chem.
283
24525-24533
2008
Homo sapiens
brenda
Agarwal, A.K.; Sukumaran, S.; Bartz, R.; Barnes, R.I.; Garg, A.
Functional characterization of human 1-acylglycerol-3-phosphate-O-acyltransferase isoform 9: cloning, tissue distribution, gene structure, and enzymatic activity
J. Endocrinol.
193
445-457
2007
Homo sapiens (Q8NF37), Homo sapiens
brenda
Schmidt, J.A.; Brown, W.J.
Lysophosphatidic acid acyltransferase 3 regulates Golgi complex structure and function
J. Cell Biol.
186
211-218
2009
Homo sapiens
brenda
Montero-Moran, G.; Caviglia, J.M.; McMahon, D.; Rothenberg, A.; Subramanian, V.; Xu, Z.; Lara-Gonzalez, S.; Storch, J.; Carman, G.M.; Brasaemle, D.L.
CGI-58/ABHD5 is a coenzyme A-dependent lysophosphatidic acid acyltransferase
J. Lipid Res.
51
709-719
2009
Homo sapiens, Mus musculus, Mus musculus (Q9DBL9)
brenda
Sukumaran, S.; Barnes, R.I.; Garg, A.; Agarwal, A.K.
Functional characterization of the human 1-acylglycerol-3-phosphate-O-acyltransferase isoform 10/glycerol-3-phosphate acyltransferase isoform 3
J. Mol. Endocrinol.
42
469-478
2009
Homo sapiens
brenda
Agarwal, A.K.; Sukumaran, S.; Cortes, V.A.; Tunison, K.; Mizrachi, D.; Sankella, S.; Gerard, R.D.; Horton, J.D.; Garg, A.
Human 1-acylglycerol-3-phosphate O-acyltransferase isoforms 1 and 2: biochemical characterization and inability to rescue hepatic steatosis in Agpat2(-/-) gene lipodystrophic mice
J. Biol. Chem.
286
37676-37691
2011
Homo sapiens (O15120), Homo sapiens (Q99943), Homo sapiens
brenda
Agarwal, A.K.; Garg, A.
Enzymatic activity of the human 1-acylglycerol-3-phosphate-O-acyltransferase isoform 11: upregulated in breast and cervical cancers
J. Lipid Res.
51
2143-2152
2010
Homo sapiens (Q7L5N7), Homo sapiens
brenda
Prasad, S.S.; Garg, A.; Agarwal, A.K.
Enzymatic activities of the human AGPAT isoform 3 and isoform 5: localization of AGPAT5 to mitochondria
J. Lipid Res.
52
451-462
2011
Homo sapiens (Q9NRZ7), Homo sapiens (Q9NUQ2), Homo sapiens
brenda
Rastegar, F.; Gao, J.L.; Shenaq, D.; Luo, Q.; Shi, Q.; Kim, S.H.; Jiang, W.; Wagner, E.R.; Huang, E.; Gao, Y.; Shen, J.; Yang, K.; He, B.C.; Chen, L.; Zuo, G.W.; Luo, J.; Luo, X.; Bi, Y.; Liu, X.; Li, M.; Hu, N.; Wang, L.; Luther, G.; Luu, H.H.; Haydon, R.C.; He, T.C.
Lysophosphatidic acid acyltransferase beta (LPAATbeta) promotes the tumor growth of human osteosarcoma
PLoS ONE
5
e14182
2010
Homo sapiens (O15120), Homo sapiens
brenda
Blaskovich, M.A.; Yendluri, V.; Lawrence, H.R.; Lawrence, N.J.; Sebti, S.M.; Springett, G.M.
Lysophosphatidic acid acyltransferase beta regulates mTOR signaling
PLoS ONE
8
e78632
2013
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
158438-158448
2020
Homo sapiens (O15120), Homo sapiens (Q99943), Homo sapiens (Q9NRZ5), Homo sapiens (Q9NRZ7), Homo sapiens (Q9NUQ2), Mus musculus (O35083), Mus musculus (Q8K3K7)
brenda