|Reactivity||Human, Mouse, Rat|
|Calculated MW||35757 Da|
|Homology||Mouse- identical; human 13/16 amino acid residues identical.|
|Other Names||Melanocortin receptor 3, MC3-R, Mc3r|
|Related products for control experiments||Control peptide antigen (supplied with the antibody free of charge).|
|Target/Specificity||Peptide (C)NSDSLTLEDQFIQHMD, corresponding to amino acid residues 102-117 ofֲ rat MC3R (Accession P32244). 1st extracellular loop.|
|Peptide Confirmation||Confirmed by mass-spectrography analysis.|
|Format||Affinity purified antibody, lyophilized powder|
|Reconstitution||50 µl or 0.2 ml deionized water, depending on the sample size.|
|Antibody Concentration After Reconstitution||0.8 mg/ml.|
|Buffer After Reconstitution||Phosphate buffered saline (PBS), pH 7.4, 1% BSA, 0.025% NaN3.|
|Storage Before Reconstitution||Lyophilized powder can be stored intact at room temperature for several weeks. For longer periods, it should be stored at -20°C.|
|Storage After Reconstitution||The reconstituted solution can be stored at 4ºC for up to 2 weeks. For longer periods, small aliquots should be stored at -20ºC or below. Avoid multiple freezing and thawing. The further dilutions should be made using a carrier protein such as BSA (1%). Centrifuge all antibody preparations before use (10000 × g 5 min).|
|Control Antigen Storage Before Reconstitution||Lyophilized powder can be stored intact at room temperature for several weeks. For longer periods, it should be stored at -20°C.|
|Control Antigen Reconstitution||100 µl water.|
|Control Antigen Storage After Reconstitution||-20ºC.|
|Preadsorption Control||1 µg peptide per 1 µg antibody.|
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Provided below are standard protocols that you may find useful for product applications.
Melanocortin Receptor 3 (MC3R) 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-, ß-, and γ-melanocyte-stimulating hormone (α-, ß-, 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 presence 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 and AGRP) with differing affinities. MC3R is the only one of the melanocortin receptors that shows no difference in binding specificity for any of the melanocortins, binding all of them with equal efficiency. AGRP is the high affinity endogenous antagonist of MC3R.1,2,3 The physiological function of MC3R is still poorly understood. The distribution of MC3R in hypothalamic nuclei of the central nervous system (CNS) suggests a role in the regulation of energy homeostasis. Indeed, studies with MC3R knockout (MC3R KO) mice showed that these mice have increased body fat due to increased feed efficiency.4 In humans, several polymorphisms of the MC3R gene are associated with high insulin levels and obesity in children.5 In addition, expression of MC3R in macrophages is thought to mediate the well known anti-inflammatory effects of α-MSH.6 Abgent is pleased to offer a highly specific antibody directed against an epitope in the extracellular first loop of rat MC3R. Anti-Melanocortin Receptor 3 (extracellular) antibody (#AG1212) can be used in Western blot, immunohistochemical, and flow cytometry applications, and recognizes MC3R from human, mouse, and rat samples.
References 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. Butler, A.A. et al. (2000) Endocrinology 141, 3518. 5. Feng, N. et al. (2005) Diabetes 54, 2663. 6. Catania, A. et al. (2004) Pharmacol. Rev. 56, 1.
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