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| Cat.No | ACP22459 | Target Name | LDLR |
|---|---|---|---|
| Form | Lyophilized powder | Expression System | Custom Production. Please inquire and provide the desire expression system. |
| Protein Length | Partial | Purity | >85% (SDS-PAGE) |
| Storage Buffer | 5%-50% glycerol. Lyophilized powder form: the buffer before lyophilization is Tris/PBS-based buffer, 6% Trehalose, Liquid form: default storage buffer is Tris/PBS-based buffer, pH 8.0. |
| Target Species | Human | Uniprot ID | P01130 |
|---|
Uniprot Id
P01130
Target Species
Human
Target Name
LDLR
Target Full Name
Low-density lipoprotein receptor
Target Function
Binds LDL, the major cholesterol-carrying lipoprotein of plasma, and transports it into cells by endocytosis. In order to be internalized, the receptor-ligand complexes must first cluster into clathrin-coated pits.; (Microbial infection) Acts as a receptor for hepatitis C virus in hepatocytes, but not through a direct interaction with viral proteins.; (Microbial infection) Acts as a receptor for Vesicular stomatitis virus.; (Microbial infection) In case of HIV-1 infection, may function as a receptor for extracellular Tat in neurons, mediating its internalization in uninfected cells.
Target Involvement
Familial hypercholesterolemia (FH)
Target Subcellular Location
Cell membrane; Single-pass type I membrane protein. Membrane, clathrin-coated pit. Golgi apparatus. Early endosome. Late endosome. Lysosome.
Target Protein Families
LDLR family
Target Synonyms
FH; FHC; LDL R; LDL receptor; LDLCQ2; Ldlr; LDLR_HUMAN; Low Density Lipoprotein Receptor; Low density lipoprotein receptor class A domain containing protein 3; Low density lipoprotein receptor familial hypercholesterolemia; Low-density lipoprotein receptor
Target Background
The low density lipoprotein receptor (LDLR) gene family consists of cell surface proteins involved in receptor-mediated endocytosis of specific ligands. The encoded protein is normally bound at the cell membrane, where it binds low density lipoprotein/cholesterol and is taken into the cell. Lysosomes release the cholesterol, which 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.
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