| Product Name | Anti-Human LDL Receptor Monoclonal Antibody |
|---|---|
| Description | 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 reciprocal stimulation of cholesterol ester synthesis takes place. Mutations in this gene cause the autosomal dominant disorder, familial hypercholesterolemia. Alternate splicing results in multiple transcript variants. Mouse Monoclonal Antibody to Human LDL Receptor |
| Synonyms | FH, FHC, LDLCQ2 |
| Clonality | Monoclonal |
| Clone | IgG-C7 |
| Immunogen | Purified bovine adrenal cortex LDL receptor |
| Isotype | IgG2b kappa |
| Specificity | Suitable for analysis of LDL receptor function in patients with familial hypercholesterolemia. The antibody recognizes an epitope in the region of repeat #1 of the ligand binding region. Addition of 15 nM antibody results in inhibition of half-maximal LDL-binding (cf. Beisiegel et al. 1981). In human normal fibroblasts the antibody detects the 160 kD polypeptide (pI 4.3) and also in bovine adrenal gland (160 kD; pI 4.6) of LDL receptors (Beisiegel et al. 1982) |
| Reactivity | Bovine, Canine, Hamster, Human, Mouse, Rabbit |
| Applications | FACS, IF, WB |
| Form | Affinity purified |
| Storage | 2-8C for immediate use, or at -2°C (aliquot) |
| References | Beisiegel U. et al. (1981) Biol Chem Vol. 22: 11923-11931Beisiegel, U. et al. (1982) J. Biol. Chem 257: 13150-13156Schmitz, G. et al. (1993) Arteiosclerosis & Thrombosis 13: 1053-1065Virgolini, I. et al. (1995) Arteiosclerosis , Thrombosis & Vascular Biology 15: 17-26 |
| Background | 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 reciprocal stimulation of cholesterol ester synthesis takes place. Mutations in this gene cause the autosomal dominant disorder, familial hypercholesterolemia. Alternate splicing results in multiple transcript variants. |
| Supplier | ARP |
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