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Lecithin-cholesterol acyltransferase

LCAT, lecithin-cholesterol acyltransferase
This gene encodes the extracellular cholesterol esterifying enzyme, lecithin-cholesterol acyltransferase. The esterification of cholesterol is required for cholesterol transport. Mutations in this gene have been found to cause fish-eye disease as well as LCAT deficiency. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: HDL, HAD, Apo, apolipoprotein A-I, CETP
Papers using LCAT antibodies
Free androgen index is superior to total testosterone for short-term assessment of the gonadal axis after renal transplantation
McMaster W. Robert et al., In Molecular & Cellular Proteomics : MCP, 2004
... LCATphosphatidylcholine-sterol acyltransferaseMBL ...
Papers on LCAT
A patient with familial amyotrophic lateral sclerosis associated with a new valosin-containing protein (VCP) gene mutation.
Ugawa et al., Fukushima, Japan. In Rinsho Shinkeigaku, Jan 2016
The other gene analysis also disclosed a known homozygous LCAT mutation (c.101C>T (p.P10L)).
Agonistic Human Antibodies Binding To Lecithin-Cholesterol Acyltransferase Modulate High Density Lipoprotein Metabolism.
Zhou et al., United States. In J Biol Chem, Jan 2016
Here we report an innovative scheme of discovery and characterization of human antibodies capable of binding to and agonizing a circulating enzyme lecithin cholesterol acyltransferase (LCAT).
Histiocytic and Nonhistiocytic Glomerular Lesions: Foam Cells and Their Mimickers.
Sethi et al., Rochester, United States. In Am J Kidney Dis, Dec 2015
We have observed this histiocytic/foamy glomerular change on the kidney biopsy specimen in 5 different disease entities: crystal-storing histiocytosis, histiocytic glomerulopathy associated with macrophage-activating syndrome, thrombotic microangiopathy, lecithin-cholesterol acyltransferase deficiency, and lipoprotein glomerulopathy.
A complex phenotype in a child with familial HDL deficiency due to a novel frameshift mutation in APOA1 gene (apoA-IGuastalla).
Bertolini et al., Genova, Italy. In J Clin Lipidol, Nov 2015
We sequenced the candidate genes for HTG (LPL, APOC2, APOA5, GPIHBP1, LMF1) and HDL deficiency (LCAT, ABCA1 and APOA1), analyzed HDL subpopulations, measured cholesterol efflux capacity (CEC) of sera and constructed a model of the mutant apoA-I.
Co-existence of classic familial lecithin-cholesterol acyl transferase deficiency and fish eye disease in the same family.
Bhardwaj et al., New Delhi, India. In Indian J Nephrol, Nov 2015
We report a family with a rare genetic disorder arising out of mutation in the gene that encodes for the enzyme lecithin-cholesterol acyltransferase (LCAT).
Implications of reverse cholesterol transport: recent studies.
Wagner et al., Louisville, United States. In Clin Chim Acta, Feb 2015
CONCLUSIONS: Mutation studies of ABCA1, LCAT and SR-B1 genes in humans showed expected variations in HDLC but little association with ASCVD and there was no significant association between HDLC and ASCVD in Mendelian randomization studies.
Paraoxonase 1 and HDL maturation.
Menini et al., Vallejo, United States. In Clin Chim Acta, Feb 2015
PON1 activation and flux across HDL particles are blocked by CETP and LCAT inhibitors.
HDL biogenesis, remodeling, and catabolism.
Chroni et al., Boston, United States. In Handb Exp Pharmacol, 2014
The biogenesis of HDL initially requires functional interaction of apoA-I with the ATP-binding cassette transporter A1 (ABCA1) and subsequently interactions of the lipidated apoA-I forms with lecithin/cholesterol acyltransferase (LCAT).
High-density lipoprotein metabolism, composition, function, and deficiency.
Asztalos et al., Boston, United States. In Curr Opin Lipidol, 2014
PURPOSE OF REVIEW: To examine the recent advances in our knowledge of HDL metabolism, composition, function, and coronary heart disease (CHD), as well as marked HDL deficiency states because of mutations in the apolipoprotein (apo) A-I, ATP-binding cassette transfer protein A1 and lecithin cholesterol acyltransferase (LCAT) gene loci.
HDL genetic defects.
Jain et al., London, United Kingdom. In Curr Pharm Des, 2013
Tangier disease and Fish Eye disease are caused by mutations in the ATP binding cassette A1 (ABCA1), a transport protein, and lecithin cholesterol acyl transferase (LCAT), an enzyme, involved in the esterification of cholesterol, respectively.
Lecithin:cholesterol acyltransferase deficiency protects against cholesterol-induced hepatic endoplasmic reticulum stress in mice.
Ng et al., Toronto, Canada. In J Biol Chem, 2012
Lecithin:cholesterol acyltransferase deficiency protects against cholesterol-induced hepatic endoplasmic reticulum stress in mice.
Genetic lecithin:cholesterol acyltransferase deficiency and cardiovascular disease.
Franceschini et al., Milano, Italy. In Atherosclerosis, 2012
This review focuses on mutations in the LCAT gene as cause of familial hypoalphalipoproteinemia, and on their impact on plasma HDL-C, HDL profile and coronary heart disease.
The role of HDL and its modulators in the development of diabetes.
Saw et al., In Curr Opin Lipidol, 2012
Studies indicate the direct effects of HDL and its major modulators, ATP-binding cassette transporter A1 (ABCA1), apolipoprotein A-I (ApoA-I), and lecithin cholesterol acyltransferase (LCAT) on the development of type 2 diabetes mellitus (T2D).
LCAT, HDL cholesterol and ischemic cardiovascular disease: a Mendelian randomization study of HDL cholesterol in 54,500 individuals.
Frikke-Schmidt et al., Copenhagen, Denmark. In J Clin Endocrinol Metab, 2012
Low plasma HDL cholesterol levels robustly associated with increased risk of MI but genetically decreased HDL cholesterol did not.
Carriers of lecithin cholesterol acyltransferase gene mutations have accelerated atherogenesis as assessed by carotid 3.0-T magnetic resonance imaging [corrected].
Stroes et al., Amsterdam, Netherlands. In J Am Coll Cardiol, 2012
Carriers of LCAT gene mutations exhibit increased carotid atherosclerosis
Hepatocyte nuclear factor-1alpha is an essential regulator of bile acid and plasma cholesterol metabolism.
Stoffel et al., New York City, United States. In Nat Genet, 2001
This is most likely due to reduced activity of the HDL-catabolic enzyme hepatic lipase (Lipc) and increased expression of HDL-cholesterol esterifying enzyme lecithin:cholesterol acyl transferase (Lcat).
Assignment of Tangier disease to chromosome 9q31 by a graphical linkage exclusion strategy.
Assmann et al., Münster, Germany. In Nat Genet, 1998
In contrast to two other monogenic HDL deficiencies in which defects in the plasma proteins apoA-I and LCAT interfere primarily with the formation of HDL (refs 7-10), TD shows a defect in cell signalling and the mobilization of cellular lipids.
Cloning and sequencing of human cholesteryl ester transfer protein cDNA.
Lawn et al., In Nature, 1987
Catalysed steps of this pathway are believed to include an efflux from peripheral cells, which generates a diffusion gradient between these membranes and extracellular fluid; esterification of this cholesterol by lecithin-cholesterol acyltransferase (LCAT) (phosphatidylcholine-sterol acyltransferase) acting on species of high-density lipoproteins; transfer of the cholesteryl esters formed (largely to low- and very low-density lipoproteins) (LDL and VLDL) by a cholesteryl ester transfer protein (CETP); and removal of these lipoproteins, together with their cholesteryl ester content, by the liver through receptor-mediated and nonspecific endocytosis.
An inherited polymorphism in the human apolipoprotein A-I gene locus related to the development of atherosclerosis.
Breslow et al., In Nature, 1983
This apoprotein serves as a cofactor for the plasma lecithin-cholesterol acyltransferase (LCAT) enzyme responsible for the formation of most cholesteryl esters in plasma, and also promotes cholesterol efflux from cells.
Familial deficiency of apolipoproteins A-I and C-III and precocious coronary-artery disease.
Alaupovic et al., In N Engl J Med, 1982
The activity of lecithin-cholesterol acyltransferase was 40 per cent of normal.
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