LDLR transports extracellular CR:atREs to cytosol

Stable Identifier
Reaction [transition]
Homo sapiens
Circulating chylomicron remnants can be directly cleared by the LDL receptor
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Chylomicron remnants (CRs) are "sieved" when they arrive at the liver by size, the appropriate sized remnants passing through the space of Disse. Once inside, CRs containing all-trans-retinyl esters (atREs) can be directly and rapidly taken up by liver parenchymal cells via the low-density lipoprotein receptor (LDLR) using apolipoprotein E (apoE) as a ligand. Internalization of remnants occur via endocytosis (see review D'Ambrosio et al. 2011). This reaction is inferred from uptake studies in mice (Yu et al. 2000). Defects in LDLR cause familial hypercholesterolemia (FH, MIM:143890), a common autosomal disease that affects about 1 in 500 people in most countries. Abnormal LDLR doesn't remove LDL from circulation resulting in high levels of LDL in blood, leading to early cardiovascular disease via atherosclerosis. The defect was first described by Brown and Goldstein (1974).

Literature References
PubMed ID Title Journal Year
11060341 Rapid initial removal of chylomicron remnants by the mouse liver does not require hepatically localized apolipoprotein E

Chen, W, Cooper, AD, Yu, KC, Jiang, Y

J. Lipid Res. 2000
Catalyst Activity

low-density lipoprotein particle receptor activity of LDLR [plasma membrane]

Inferred From
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