The low density lipoprotein receptor (LDL-R) 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-methylglutarylcoenzyme A (HMG CoA) reductase, the rate-limiting step in cholesterol synthesis. At the same time, a reciprocal stimulation of cholesterol ester synthesis takes place. Mutations in the LDL-R gene cause the autosomal dominant disorder, familial hypercholesterolemia. Along with SCARB1, CLDN1, and the tetraspanin superfamily member CD81, LDL-R has been reported to be an entry factor for the Hepatitis C virus. At least three isoforms of LDL-R are known to exist.
Samples:
FFPE tissue
Target:
Human LDLR
IHC0438H
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