EC Number   |
General Information |
Reference |
|---|
   2.3.1.43 | evolution |
LCAT is a member of the alpha/beta hydrolase family |
737191 |
| 2.3.1.43 | evolution |
lysosomal phospholipase A2 (LPLA2) and lecithin:cholesterol acyltransferase (LCAT) belong to a structurally uncharacterized family of key lipid-metabolizing enzymes responsible for lung surfactant catabolism and for reverse cholesterol transport, respectively. LCAT has a close structural relationship to LPLA2, construction of an LPLA2-based homology model corresponding to the catalytic, membrane binding and cap domains of LCAT, structure comparisons, overview. Lys202 in the alpha3 helix and Thr329 in the catalytic domain are invariant in LPLA2 and LCAT, but are conserved as hydrophobic residues in bacterial lipases. Although LPLA2 exhibits structural homology with bacterial lipases, their substrates are fundamentally different in that LPLA2 and LCAT hydrolyse glycerophospholipids, which contain polar, charged head groups, instead of triacylglycerol |
736865 |
| 2.3.1.43 | malfunction |
a high LCAT level is associated with an increased coronary artery disease risk in women |
705010 |
| 2.3.1.43 | malfunction |
deficiency in LCAT sensitizes mice to diet-induced hepatic deposition of triglycerides and alterations in hepatic histology and architecture. Mechanistic analysis indicate that this is due to enhanced intestinal absorption of dietary triglycerides, accelerated clearance of postprandial triglycerides from the circulation and reduced rate of hepatic triglyceride secretion. Ectopic expression of human LCAT by gene transfer in LCAT-/- mice fed a Western-type diet for 12 weeks result in a significant reduction in their hepatic triglyceride content and a great improvement of hepatic histology and architecture |
720298 |
| 2.3.1.43 | malfunction |
enzyme mutations and loss of enzyme activity are involved in several diseases, e.g. atherosclerosis and acute coronary syndrome |
736865 |
| 2.3.1.43 | malfunction |
homozygosity for loss-of-function mutations causes familial lecithin-cholesterol acyltransferase deficiency, characterized by corneal opacities, anemia, and renal involvement |
755762 |
| 2.3.1.43 | malfunction |
inborn enzyme deficiency leads to the fish-eye disease, as well as anemia, proteinuria, renal failure, hepatosplenomegaly, and lymphadenopathy |
703346 |
| 2.3.1.43 | malfunction |
LCAT deficiency is involved in the end-stage renal insufficiency with elevated plasma triglyceride concentration, reduced and plasma HDL cholesterol, apolipoprotein A-1 and LCAT concentrations, whereas plasma phospholipid transfer protein and cholesteryl ester transfer protein concentrations and activities are unchanged in the patients |
705896 |
| 2.3.1.43 | malfunction |
LCAT inhibition leads to the Balkan endemic nephropathy, BEN, chronic, slowly progressive renal disease, overview. Familial renal disease can develop secondary LCAT deficiency and associated lipid abnormalities |
703789 |
| 2.3.1.43 | malfunction |
LCAT is synthesized in the liver and its synthesis and/or excretion is impaired in hepatocellular diseases as indicated by decreased activity of LCAT, e.g. parturient-haemoglobinuria and ketosis, detection of ketonuria, induced phenotypes, overview |
706707 |
