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LDLR |
LOCUS ID | 3949 | ||||||||||||||||
GENE_SYMBOL | LDLR | ||||||||||||||||
GENE NAME | low density lipoprot | ||||||||||||||||
SYNONYMNS | FH, FHC, LDLCQ2 | ||||||||||||||||
CHROMOSOME | 19 | ||||||||||||||||
HOMOLOGENE ID | 55469 |
microRNAs | NA | NA |
GENE SUMMARY |
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The low density lipoprotein receptor (LDLR) gene family consists of cell surface proteins involved in receptor-mediated endocytosis of specific ligands. Low density lipoprotein (LDL) is normally bound at the cell membrane and taken into the cell ending up in lysosomes where the protein is degraded and the cholesterol is made available for repression of microsomal enzyme 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase, the rate-limiting step in cholesterol synthesis. At the same time, a |
OBSERVATIONS |
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Complication | Evidence | PMID |
Cardiovascular | 1. In , because various genes, LDLR, CETP, APOA5, Apo E, Apo B, and Apo A-I, are associated with the precipitation of CAD associated with T2DM, a personalized diet-gene intervention therapy may be advocated to reduce the disease precipitation. | 25470794 |
Atherosclerosis | 1. Cardiovascular complications are the leading cause of mortality in type 2 diabetes (T2DM), in which onset and progression of atherosclerosis is linked to chronic inflammation. Activation status of innate immune cells (granulocytes [Gc], monocytes [Mc]), as reflected by increased CD11b, CD66b, and other surface markers, increases their endothelial and cytokinechemokines release | 23686079 |
Insulin resistance and inflammation | 1. The greater rate of hepatic cholesterol synthesis in obese individuals suppresses the expression of hepatic LDL receptors (LDLR), thereby reducing hepatic LDL uptake. | 22332058 |