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Details on Person Chylomicron remnants (CRs) are "sieved" when they arrive at ...
| Class:Id | Summation:2424271 |
|---|---|
| _displayName | Chylomicron remnants (CRs) are "sieved" when they arrive at ... |
| _timestamp | 2012-11-15 09:43:13 |
| created | [InstanceEdit:2424261] Jassal, B, 2012-07-23 |
| literatureReference | [LiteratureReference:2425425] Vitamin A metabolism: an update [LiteratureReference:2426086] Familial hypercholesterolemia: defective binding of lipoproteins to cultured fibroblasts associated with impaired regulation of 3-hydroxy-3-methylglutaryl coenzyme A reductase activity |
| modified | [InstanceEdit:2424279] Jassal, B, 2012-07-23 [InstanceEdit:2425431] Jassal, B, 2012-07-25 [InstanceEdit:2426097] Jassal, B, 2012-07-25 [InstanceEdit:2429684] Jassal, B, 2012-08-09 [InstanceEdit:2534412] Jassal, Bijay, 2012-10-26 [InstanceEdit:2586567] Jassal, B, 2012-11-15 |
| text | 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). |
| (summation) | [Reaction:2424254] LDLR transports extracellular CR:atREs to cytosol [Homo sapiens] |
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No pathways have been reviewed or authored by Chylomicron remnants (CRs) are "sieved" when they arrive at ... (2424271)
