LDLR

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LDLR

A gene on chromosome 19p13.2 that encodes a cell surface protein involved in receptor-mediated endocytosis of low-density lipoprotein (LDL), the major cholesterol-carrying lipoprotein of plasma, which it transports into cells by endocytosis. Internalisation of the receptor-ligand complex requires clustering into clathrin-coated pits.
References in periodicals archive ?
The PCSK9 [6] gene (proprotein convertase subtilisin/ kexin type 9) encodes an enzyme that is involved in regulating the degradation of the LDL receptor protein in the lysosome of the cell, preventing it from being recycled to the cell surface (1, 2).
The normal role of the PCSK9 protein is to break down the LDL receptor (LDL-R); when there is less PCSK9 protein, there is more LDL-R on the cell surface.
Apo B-100 is essential for the binding of LDL particles to the LDL receptor (LDLR) for cellular uptake and degradation (2).
The LDL receptor relative with 11 ligand-binding repeats (LR11) [4] (also known as SorLA) (1, 2) is a member of the LDL receptor family and is highly expressed in atheromatous plaques, particularly in the intimal smooth muscle cells (SMCs) at the border between the arterial intima and the media (3).
In addition to underscoring the role of high triglycerides in heart attack risk, Kathiresan and his colleagues also found that harmful LDL receptor mutations are more prevalent than previously believed - roughly twice as common than had been estimated in the Goldstein study.
Proprotein convertase subtilisin/kexin type 9 (PCSK9)6 is a key regulator of plasma LDL cholesterol concentrations by virtue of its ability to target the LDL receptor (LDLr) for degradation in the lysosome (1, 2).
Small, dense LDL particles also have a prolonged plasma half-life because of their lower binding affinity for the LDL receptor (4).
Analysis of sequence variations in the LDL receptor gene in Spain: general gene screening or search for specific alterations?
Its interaction with the LDL receptor (LDLR), LDL-receptor related protein (LRP), and VLDL receptor permits clearance of triglyceride-rich lipoprotein remnants.
Familial hypercholesterolemia (FH) (1) is an autosomal dominantly inherited disorder of lipoprotein metabolism caused by sequence variations in the LDL receptor (LDLR) (2) gene (1).
When the defect is found in the gene that codes for the LDL receptor ligand, APOB, the ADH is known as familial defective apolipoprotein B100 (FDB).