| 货号 | AMR-022-50ul |
| 描述 | Each antibody ordered from Alomone Labs is supplied with its corresponding control peptide (antigen), free of charge. A Rabbit Polyclonal Antibody to Melanocortin Receptor 2 |
| 反应种属 | H, M, R |
| 应用 | IH, WB |
| 供应商 | Alomone |
| 背景 | Melanocortin Receptor 2 (MC2R) belongs to a five-member receptor family known as the melanocortin receptors. The melanocortin receptors are members of the 7 transmembrane domain, G protein-coupled receptor (GPCR) superfamily. The receptors ligands, the melanocortins, are a group of structurally derived peptides consisting of α-, ß- and γ melanocyte stimulating hormone (α, ß, γ-MSH) and the adrenocorticotropic hormone (ACTH) all of which are derived from the post-translational processing of a common precursor peptide, proopiomelanocortin (POMC).1,2,3 One of the most salient features of the melanocortin signaling system is the presence of two endogenous antagonists, that is proteins that bind specifically to the receptor but instead of activating it have an inhibitory effect. The antagonist proteins are termed agouti (or agouti signaling protein, ASP) and agouti-related protein (AGRP).4 All five melanocortin receptors bind their agonists (the melanocortins) and their endogenous antagonists (agouti and AGRP) with different affinities. MC2R can be also described as the ACTH receptor as it is exclusively activated by the ACTH hormone. In fact, MC2R mediates all the physiological effects of ACTH in the adrenal cortex, that is the regulation and production of steroids, their circadian variation and their stress-related fluctuations.1, 2, 3 In addition, mutations that result in MC2R functional impairment are associated with familial glucocorticoid deficiency.4 The receptor transduces signals via Gs resulting in the activation of adenylate cyclase and production of cAMP. |
| 运输条件 | Ambient |
| 存放说明 | -20 |
| 纯度 | Affinity purified on immobilized antigen. |
| 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. Endocrinol. Metab. 284,E468. 3. Wikberg, J.E.S. et al.(2000)Pharm. Res.42,393. 4. Elias, L.L. et al.(1999)J Clin Endocrinol Metab 84,2766. |
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