Melanocortin Receptor 4 (extracellular) Antibody

分子量：
36943 Da
细胞定位：

形式：
Affinity purified antibody, Liquid
参考文献：
1. Abdel-Malek, Z.A. (2001) Cell. Mol. Life Sci. 58, 434.2. Gantz, I. and Fong, T.M. (2003) Am. J. Physiol. 284, E468.3. Wikberg, J.E. et al. (2000) Pharmacol. Res. 42, 393.4. Huszar, D. et al (1997) Cell 88, 131.5. Adan, R.A. et al. (2006) Br. J. Pharmacol. 149, 815.
产品概述：
We constantly strive to ensure we provide our customers with the best antibodies. As a result of this work we offer this antibody in purified format. We are in the process of updating our datasheets. If you have any questions regarding this update, please feel free to contact our technical support team.This product is a high quality Melanocortin Receptor 4 (extracellular) antibody.
功能：

总结：
Melanocortin Receptor 4 (MC4R) is one of five members of the melanocortin receptor family, which belongs to the 7-transmembrane domain, G protein-coupled receptor (GPCR) superfamily. The ligands of these receptors, the melanocortins, are a group of structurally-related peptides comprising the α-, β-, and γ-melanocyte-stimulating hormone (α-, β-, γ-MSH) and the adrenocorticotropic hormone (ACTH), all of which are derived from post-translational processing of a common precursor peptide, proopiomelanocortin (POMC).1,2,3 One of the salient features of the melanocortin signaling system is the existence of two endogenous antagonists, proteins that bind specifically to the receptor and have an inhibitory effect. These antagonist proteins are termed agouti (or agouti signaling protein, ASP) and agouti-related protein (AGRP).1 All five melanocortin receptors bind their agonists (the melanocortins) and their endogenous antagonists (agouti/ASP and AGRP) with differing affinities. The order of potency for MC4R activation is α-MSH = ACTH > β-MSH >> γ-MSH. AGRP and agouti/ASP are both endogenous antagonists of MC4R.1,2,3 MC4R is widely expressed in the brain including the cortex, thalamus, hypothalamus, and brain stem. The best understood physiological role of MC4R is in the regulation of feeding behavior and the control of body weight. Indeed, mice with a targeted disruption of the MC4R gene display an obese phenotype characterized by increased adiposity, hyperphagia, and hyperleptinaemia.4 Similarly, MC4R mutations in humans have been associated with severe childhood obesity including characteristics very similar to the MC4R knockout mouse phenotype.5 All these make MC4R an attractive drug target for the treatment of obesity.
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