LDL-R Antibody
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application
| WB, IHC-P, IF, E |
---|---|
Primary Accession | P01130 |
Other Accession | NP_000518, 4504975 |
Reactivity | Human, Mouse, Rat |
Host | Chicken |
Clonality | Polyclonal |
Isotype | IgY |
Calculated MW | 95376 Da |
Application Notes | LDL-R antibody can be used for detection of LDL-R by Western blot at 1 - 2 µg/mL. Antibody can also be used for immunohistochemistry starting at 2.5 µg/mL. For immunofluorescence start at 20 µg/mL. |
Gene ID | 3949 |
---|---|
Target/Specificity | LDLR; |
Reconstitution & Storage | LDL-R antibody can be stored at 4℃ for three months and -20℃, stable for up to one year. As with all antibodies care should be taken to avoid repeated freeze thaw cycles. Antibodies should not be exposed to prolonged high temperatures. |
Precautions | LDL-R Antibody is for research use only and not for use in diagnostic or therapeutic procedures. |
Name | LDLR |
---|---|
Function | Binds low density lipoprotein /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. Forms a ternary complex with PGRMC1 and TMEM97 receptors which increases LDLR-mediated LDL internalization (PubMed:30443021). |
Cellular Location | Cell membrane; Single-pass type I membrane protein {ECO:0000250|UniProtKB:P01131}. Membrane, clathrin-coated pit. Golgi apparatus. Early endosome. Late endosome. Lysosome Note=Rapidly endocytosed upon ligand binding. Localized at cell membrane, probably in lipid rafts, in serum-starved conditions (PubMed:30443021). |
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Provided below are standard protocols that you may find useful for product applications.
Background
LDL-R Antibody: 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-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 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.
References
Li Y, Cam J, and Bu G. Low-density lipoprotein receptor family: endocytosis and signal transduction. Mol. Neurobiol.2001; 23:53-67.
Austin MA, Hutter CM, Zimmern RL, et al. Familial hypercholesterolemia and coronary heart disease: a HuGE association review. Am. J. Epidemiol.2004; 160:421-9.
Helle F and Dubuisson J. Hepatitis C virus entry into host cells. Cell Mol. Life Sci.2008; 65:100-12.
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