LCAT
LCAT (lecithin-cholesterol acyltransferase, also named phosphatidylcholine-sterol acyltransferase) is a secreted enzyme central to the extracellular metabolism of plasma lipoproteins. It esterifies cholesterol on the surface of HDL and LDL particles, supporting cholesterol transport back to the liver. Browse Assay Genie's current range of LCAT research reagents below, or read on for the biology behind the target.
LCAT is synthesised mainly in the liver and secreted into plasma, where it converts cholesterol and phosphatidylcholines (lecithins) to cholesteryl esters and lysophosphatidylcholines on the surface of high and low density lipoproteins (HDLs and LDLs). The cholesterol ester is then transported back to the liver. The enzyme shows a preference for plasma 16:0-18:2 or 18:O-18:2 phosphatidylcholines, and it is required for remodelling HDL particles into their spherical forms.
Beyond plasma lipoprotein metabolism, LCAT is also produced in the brain by primary astrocytes. There it esterifies free cholesterol on nascent APOE-containing lipoproteins secreted from glia and influences cerebrospinal fluid APOE and APOA1 levels. Together with APOE and the cholesterol transporter ABCA1, it plays a key role in the maturation of glial-derived, nascent lipoproteins. LCAT also catalyses the hydrolysis of platelet-activating factor (PAF) to lyso-PAF, transfers the acetate group from PAF to 1-hexadecanoyl-sn-glycero-3-phosphocholine to form lyso-PAF, and esterifies (24S)-hydroxycholesterol (cerebrosterol) to produce monoesters.
The LCAT gene encodes this extracellular cholesterol-esterifying enzyme, which belongs to the AB hydrolase superfamily and the lipase family. HGNC places it in the acyltransferases gene group, and orthologues are annotated in mouse and rat (Lcat). Mutations in the LCAT gene have been found to cause fish-eye disease as well as LCAT deficiency, making the protein a focus for lipoprotein and cholesterol transport research.
LCAT is a central enzyme in extracellular plasma lipoprotein metabolism, esterifying cholesterol on HDL and LDL particles.
Cholesterol esterification by LCAT is required for cholesterol transport, with cholesteryl esters carried back to the liver.
Astrocyte-derived LCAT acts with APOE and ABCA1 in maturing glial lipoproteins and influences CSF APOE and APOA1 levels.
Mutations in the LCAT gene cause fish-eye disease and LCAT deficiency, making it relevant to genetic dyslipidaemia studies.
LCAT is secreted mainly by the liver into plasma, where it converts cholesterol and phosphatidylcholines to cholesteryl esters and lysophosphatidylcholines on HDL and LDL surfaces. The cholesterol ester is then transported back to the liver. It also remodels HDL particles into spherical forms and acts on platelet-activating factor.
The HGNC full name is lecithin-cholesterol acyltransferase, while UniProt lists the protein as phosphatidylcholine-sterol acyltransferase. No alternative gene symbols or previous symbols are recorded. The enzyme carries the EC number 2.3.1.43 and belongs to the acyltransferases gene group.
Mutations in the LCAT gene have been found to cause fish-eye disease and LCAT deficiency. Orthologues are annotated in mouse and rat, both named Lcat. Check the datasheet of any product for its validated reactivity.
Lipoprotein partners and cholesterol transport proteins connected to LCAT biology, including APOE, APOA1 and ABCA1.
Gene and protein annotations from HGNC, NCBI Gene and UniProt P04180; product specifications from Assay Genie datasheets.