LDLR

(redirected from low-density lipoprotein receptor)

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 ?
Repatha (evolocumab) is a human monoclonal antibody that binds to proprotein convertase subtilisin/kexin type 9 (PCSK9) and inhibits circulating PCSK9 from binding to the low-density lipoprotein receptor (LDLR), preventing PCSK9-mediated LDLR degradation and permitting LDLR to recycle back to the liver cell surface.
Exemplar Genetics announced the FDA exercised enforcement discretion in regard to its ExeGen low-density lipoprotein receptor miniswine, clearing this animal that enables superior translational research and better predictive efficacy for commercial use as a research model.
First case report of familial hypercholesterolemia in an Omani family due to novel mutation in the low-density lipoprotein receptor gene.
High prevalence of a novel mutation in the exon 4 of the low-density lipoprotein receptor gene causing familial hypercholesterolemia in Belgium.
2005) [14], their study also shows that tendon xanthomas in familial hypercholesterolemia are associated with cardiovascular risk independent of low-density lipoprotein receptor gene mutation.
Familial hypercholesterolemia (FH) is caused by mutations in the genes coding for the low-density lipoprotein receptor (LDLR), apolipoprotein B-lOO, or proprotein convertase subtilisin/kexin type 9 (PCSK9).
Dysfunction of BBB receptors that transport beta-amyloid out of the brain: Studies suggest that AD is associated with the malfunction of low-density lipoprotein receptor related protein-1 (LRP), a blood-brain barrier transporter that prevents the buildup of beta-amyloid by binding to it and removing it from the brain.
PCSK9 disrupts the activity of a key molecule called the low-density lipoprotein receptor, or LDLR, which is made and secreted in the liver.
Depletion of natural killer cell function decreases atherosclerosis in low-density lipoprotein receptor null mice.
Colesevelam significantly increased hepatic gene expression for scavenger receptor type BI, apolipoprotein A1, LCAT, cholesterol ester transfer protein, cholesterol 7-[alpha]-hydroxylase (CYP7A1), low-density lipoprotein receptor, and liver X receptor (LXR).
Contrary to the accepted hypothesis positing downregulation of low-density lipoprotein receptor (LDLR) in humans, expression of the human APOE4 isoform combined with increased LDLR was harmful in genetically modified mice when red a high-fat Western diet, predicting important interactions between genotype/phenotype and exposure.

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