2.3.1.43: phosphatidylcholine-sterol O-acyltransferase
This is an abbreviated version!
For detailed information about phosphatidylcholine-sterol O-acyltransferase, go to the full flat file.
Word Map on EC 2.3.1.43
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2.3.1.43
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lipoprotein
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hdl
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apolipoproteins
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cholesteryl
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high-density
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triglyceride
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esterification
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apoa-i
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atherosclerosis
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lipase
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esterify
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low-density
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coronary
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cardiovascular
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hdl-cholesterol
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unesterified
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opacity
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apoproteins
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hypercholesterolemia
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corneal
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discoidal
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atherogenic
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subfractions
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hdl-associated
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triglyceride-rich
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apoc-iii
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postheparin
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synthesis
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hyperlipoproteinemia
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lysolecithin
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vldl-c
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tg-rich
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dimyristoyl
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antiatherogenic
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b-containing
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normolipidemic
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cholesterol-loaded
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xanthoma
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medicine
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lipoprotein-cholesterol
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chylomicron
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acyl-coa:cholesterol
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lipid-free
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paraoxonase
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apob-containing
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hdl-mediated
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3hcholesterol
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drug development
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lipid-poor
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hypertriglyceridemia
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tangier
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very-low-density
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non-hdl
- 2.3.1.43
- lipoprotein
- hdl
-
apolipoproteins
-
cholesteryl
-
high-density
- triglyceride
- esterification
- apoa-i
- atherosclerosis
- lipase
-
esterify
-
low-density
- coronary
- cardiovascular
-
hdl-cholesterol
-
unesterified
- opacity
- apoproteins
- hypercholesterolemia
- corneal
-
discoidal
-
atherogenic
-
subfractions
-
hdl-associated
-
triglyceride-rich
- apoc-iii
-
postheparin
- synthesis
- hyperlipoproteinemia
- lysolecithin
-
vldl-c
-
tg-rich
-
dimyristoyl
-
antiatherogenic
-
b-containing
-
normolipidemic
-
cholesterol-loaded
-
xanthoma
- medicine
-
lipoprotein-cholesterol
- chylomicron
-
acyl-coa:cholesterol
-
lipid-free
- paraoxonase
-
apob-containing
-
hdl-mediated
-
3hcholesterol
- drug development
-
lipid-poor
- hypertriglyceridemia
- tangier
-
very-low-density
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non-hdl
Reaction
Synonyms
acyltransferase, lecithin-cholesterol, cholesterol transacyltransferase, LAT, LCAT, lecithin cholesterol acyl transferase, lecithin cholesterol acyltransferase, lecithin-cholesterol acyl transferase, lecithin-cholesterol acyltransferase, lecithin/cholesterol acyltransferase, lecithin: cholesterol acyltransferase, lecithin:cholesterol acyl-transferase, lecithin:cholesterol acyltransferase, lysolecithin acyltransferase, phospholipid-cholesterol acyltransferase, plasma lecithin-cholesterol acyltransferase, TgLCAT, TGME49_272420
ECTree
2.3.1.43 phosphatidylcholine-sterol O-acyltransferaseAdvanced search results
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results (Natural Substrates Products
Natural Substrates Products on EC 2.3.1.43 - phosphatidylcholine-sterol O-acyltransferase
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NATURAL SUBSTRATE 
NATURAL PRODUCT
REACTION DIAGRAM
ORGANISM
UNIPROT
COMMENTARY
(Substrate)
(Substrate)
LITERATURE
(Substrate)
(Substrate)
COMMENTARY
(Product)
(Product)
LITERATURE
(Product)
(Product)
REVERSIBILITY
r=reversible
ir=irreversible
?=not specified
r=reversible
ir=irreversible
?=not specified
phosphatidylcholine + cerebrosterol
1-acylglycerophosphocholine + cerebrosteryl ester
i.e. (24S)-hydroxycholesterol
-
-
?
phosphatidylcholine + cholesterol
1-acylglycerophosphocholine + cholesterol ester
-
-
-
?
phosphatidylcholine + cholesterol
3-acylglycerophosphocholine + ?
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isozyme abnormality cause hepatosplenic schistosomiasis mansoni, important in lipoprotein metabolism and cholesterol transport, cholesterol is trapped in the HDL particles, enzyme transfers a long-chain fatty acyl residue from the sn-2 position of phosphatidylcholine, i.e. lecithin, to the 3-beta-hydroxyl group of cholesterol producing lysophosphatidylcholine or lysolecithin and cholesteryl ester, predominantly on HDL containing the activator apolipoprotein A-I
-
-
?
phosphatidylcholine + a sterol
1-acylglycerophosphocholine + a sterol ester
-
-
-
-
?
phosphatidylcholine + a sterol
1-acylglycerophosphocholine + a sterol ester
-
-
-
?
phosphatidylcholine + a sterol
1-acylglycerophosphocholine + a sterol ester
-
-
-
-
?
phosphatidylcholine + a sterol
1-acylglycerophosphocholine + a sterol ester
-
-
-
?
phosphatidylcholine + a sterol
1-acylglycerophosphocholine + a sterol ester
-
-
-
-
?
phosphatidylcholine + a sterol
1-acylglycerophosphocholine + a sterol ester
-
-
-
?
phosphatidylcholine + a sterol
1-acylglycerophosphocholine + a sterol ester
-
-
-
?
phosphatidylcholine + a sterol
1-acylglycerophosphocholine + a sterol ester
-
-
-
?
phosphatidylcholine + cholesterol
1-acylglycerophosphocholine + cholesteryl ester
-
-
-
-
?
phosphatidylcholine + cholesterol
1-acylglycerophosphocholine + cholesteryl ester
-
-
-
?
phosphatidylcholine + cholesterol
1-acylglycerophosphocholine + cholesteryl ester
-
esterification of plasma cholesterol in HDL via alpha-enzyme activity, and of plasma cholesterol in LDL via beta-enzyme activity
-
-
?
phosphatidylcholine + cholesterol
1-acylglycerophosphocholine + cholesteryl ester
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the enzyme is responsible for esterification of cholesterol in high density lipoprotein HDL to prevent diffusion of cholesterol back to the cell
-
-
?
phosphatidylcholine + cholesterol
1-acylglycerophosphocholine + cholesteryl ester
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LCAT contributes significantly to the apoB lipoprotein cholesteryl ester pool, enzyme role in lipid and lipoprotein metabolism in plasma, detailed overview
-
-
?
phosphatidylcholine + cholesterol
1-acylglycerophosphocholine + cholesteryl ester
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LCAT contributes significantly to the apoB lipoprotein cholesteryl ester pool, enzyme role in lipid and lipoprotein metabolism in plasma, detailed overview
-
-
?
phosphatidylcholine + cholesterol
cholesteryl ester + lysophosphatidylcholine
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LCAT is a serum enzyme that catalyses esterification of free cholesterol to produce cholesteryl ester. Cholesterol for this reaction comes from peripheral tissues and the donor of the acyl group is lecithin from the high density lipoprotein, HDL, particles
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-
?
phosphatidylcholine + cholesterol
cholesteryl ester + lysophosphatidylcholine
-
-
-
-
?
phosphatidylcholine + cholesterol
cholesteryl ester + lysophosphatidylcholine
-
LCAT hydrolyzes the sn-2 acyl group of phosphatidylcholine and subsequently transfers and esterifies the fatty acid to free cholesterol with apolipoprotein A-I as cofactor
-
-
?
phosphatidylcholine + cholesterol
cholesteryl ester + lysophosphatidylcholine
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LCAT is a plasma enzyme produced by the liver, that catalyzes the conversion of cholesterol to cholesteryl esters on lipoproteins by the transacylation of fatty acid from the sn-2 position of phosphatidylcholine to the 3-hydroxyl group on the A-ring of cholesterol
-
-
?
phosphatidylcholine + cholesterol
cholesteryl ester + lysophosphatidylcholine
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LCAT is critical in the metabolism of HDL
-
-
?
phosphatidylcholine + cholesterol
cholesteryl ester + lysophosphatidylcholine
-
-
-
-
?
phosphatidylcholine + cholesterol
cholesteryl ester + lysophosphatidylcholine
-
-
-
-
?
phosphatidylcholine + sterol
1-acylglycerophosphocholine + sterol ester
-
-
-
r
phosphatidylcholine + sterol
1-acylglycerophosphocholine + sterol ester
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enzyme is believed to act on the surface of high-density lipoproteins, catalyzes the hydrolysis of fatty acids of the sn-2-position of phosphatidylcholine and transfers the fatty acid to free cholesterol to form cholesteryl ester, transesterification is the major source of plasma cholesteryl ester in human, enzyme has the key role in the transport of cholesterol from peripheral tissues to the liver, in the interconversion of HDL subclasses and the maintenance of lipoprotein structure
-
?
phosphatidylcholine + sterol
1-acylglycerophosphocholine + sterol ester
-
important in metabolism and structure of plasma lipoproteins
-
?
additional information
?
-
enzyme deficiency can cause corneal opacity, proteinuria, anemia, and kidney failure
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-
?
additional information
?
-
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enzyme deficiency can cause corneal opacity, proteinuria, anemia, and kidney failure
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-
?
additional information
?
-
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enzyme forms higher aggregates with HDL and apolipoprotein A-I in plasma, esterification of cholesterol and binding to cholesteryl ester transfer protein are required for reverse cholesterol transport from peripheral cells to plasma
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-
?
additional information
?
-
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a frameshift mutation of the LCAT gene is associated with renal failure with proteinuria, corneal opacity, and anemia in familial LCAT deficiency
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-
?
additional information
?
-
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the activity and fatty acid specificity of LCAT may be altered during the inflammatory response
-
-
?
additional information
?
-
-
the enzyme is involved in development of atherosclerosis
-
-
?
additional information
?
-
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the enzyme is responsible for the cholesterol transport, controlling the flow of cholesterol from peripheral tissues to the liver
-
-
?
additional information
?
-
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the rare enzyme genetic disorder, familial LCAT deficiency, leads to altered plasma lipid and lipoprotein levels, corneal opacities and proteinuria with renal failure, phenotype analysis, overview
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-
?
additional information
?
-
-
about 75% of plasma LCAT is associated with HDL
-
-
?
additional information
?
-
-
HDL2 and HDL3-phospholipids, HDL2-cholesterol concentrations and LCAT activity are reduced in preganancy-induced hypertension and in chronic hypertensive mothers, as well as in their small for gestational age, SGA, newborns, overview
-
-
?
additional information
?
-
-
plasma high-sensitivity C-reactive protein, CRP, is correlated inversely with HDL-C and apo A-I, and positively with LCAT activity, interaction between apo A-I and LCAT activity on CRP, interaction analysis, overview
-
-
?
additional information
?
-
cholesterol and (24S)-hydroxycholesterol compete for enzyme activity
-
-
?
additional information
?
-
structure/function requirements for the apolipoprotein A-I and lecithin cholesterol acyltransferase interaction loop of HDL, binding studies with recombinant wild/type apoA-I and apoA-I mutants P165A, Y166A, Y166E, Y166F, Y166N, S167A, D168A, Y192F, and Y192L. Loss of LCAT activation caused by apoA-I Y166A or Y166F mutations is at least partially due to the weaker binding between LCAT and apoA-I within these rHDL. Both Vmax of Y166F and Y166A are 20% lower than that of wild-type apoA-I, and the apparent Km are about 2-6fold higher than wild-type. rHDL formed with either apoA-I Y192F or Y192L mutants show normal LCAT activity. Incubation of hLCAT with rHDL formed using the apoA-I mutants P165A, Y166A, Y166F, S167A and D168A all show significant decreases in LCAT activity of 40%-60% compared with the wild-type
-
-
?
additional information
?
-
-
structure/function requirements for the apolipoprotein A-I and lecithin cholesterol acyltransferase interaction loop of HDL, binding studies with recombinant wild/type apoA-I and apoA-I mutants P165A, Y166A, Y166E, Y166F, Y166N, S167A, D168A, Y192F, and Y192L. Loss of LCAT activation caused by apoA-I Y166A or Y166F mutations is at least partially due to the weaker binding between LCAT and apoA-I within these rHDL. Both Vmax of Y166F and Y166A are 20% lower than that of wild-type apoA-I, and the apparent Km are about 2-6fold higher than wild-type. rHDL formed with either apoA-I Y192F or Y192L mutants show normal LCAT activity. Incubation of hLCAT with rHDL formed using the apoA-I mutants P165A, Y166A, Y166F, S167A and D168A all show significant decreases in LCAT activity of 40%-60% compared with the wild-type
-
-
?
additional information
?
-
-
LCAT adds cholesteryl ester to LDL in mice and is important in remodeling VLDL to LDL, LCAT deficiency significantly decreases the cholesteryl ester percentage and significantly increases the phospholipid percentage of LDL, overview
-
-
?
additional information
?
-
-
increased HDL cholesterol after LCAT lecithin-cholesterol acyltransfer activity inhibits progression of atherosclerosis and induces cholesterol unloading in complex lesions in rabbits, overview
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-
?
additional information
?
-
the enzyme from Toxoplasma gondii also shows phospholipase and hemolytic activity, recombinant TgLCAT has a dual enzymatic activity as a calcium-independent phospholipase A2 and a cholesterol transacyltransferase
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-
?
additional information
?
-
-
the enzyme from Toxoplasma gondii also shows phospholipase and hemolytic activity, recombinant TgLCAT has a dual enzymatic activity as a calcium-independent phospholipase A2 and a cholesterol transacyltransferase
-
-
?
additional information
?
-
the enzyme from Toxoplasma gondii also shows phospholipase and hemolytic activity, recombinant TgLCAT has a dual enzymatic activity as a calcium-independent phospholipase A2 and a cholesterol transacyltransferase
-
-
?
