|Application ||WB, E|
|Calculated MW||34706 Da|
|Antigen Region||205-232 aa|
|Other Names||Melanocyte-stimulating hormone receptor, MSH-R, Melanocortin receptor 1, MC1-R, MC1R, MSHR|
|Target/Specificity||This MC1R antibody is generated from mice immunized with a KLH conjugated synthetic peptide between 205-232 amino acids from the Central region of human MC1R.|
|Format||Purified monoclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is prepared by Euglobin precipitation followed by dialysis against PBS.|
|Storage||Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||MC1R Antibody (Center) is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||Receptor for MSH (alpha, beta and gamma) and ACTH. The activity of this receptor is mediated by G proteins which activate adenylate cyclase.|
|Cellular Location||Cell membrane; Multi-pass membrane protein.|
|Tissue Location||Melanocytes and corticoadrenal tissue.|
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This intronless gene encodes the receptor protein for melanocyte-stimulating hormone (MSH). The encoded protein, a seven pass transmembrane G protein coupled receptor, controls melanogenesis. Two types of melanin exist: red pheomelanin and black eumelanin. Gene mutations that lead to a loss in function are associated with increased pheomelanin production, which leads to lighter skin and hair color. Eumelanin is photoprotective but pheomelanin may contribute to UV-induced skin damage by generating free radicals upon UV radiation. Binding of MSH to its receptor activates the receptor and stimulates eumelanin synthesis. This receptor is a major determining factor in sun sensitivity and is a genetic risk factor for melanoma and non-melanoma skin cancer. Over 30 variant alleles have been identified which correlate with skin and hair color, providing evidence that this gene is an important component in determining normal human pigment variation. [provided by RefSeq].
Demenais, F., et al. J. Natl. Cancer Inst. 102(20):1568-1583(2010)
Strange, R.C., et al. Mult. Scler. 16(9):1109-1116(2010)
Ibarrola-Villava, M., et al. Exp. Dermatol. 19(9):836-844(2010)
Smith, G., et al. Pharmacogenet. Genomics (2010) In press :
Kricker, A., et al. Cancer Causes Control (2010) In press :
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