|Application ||WB, IHC, ICC|
|Reactivity||Human, Mouse, Rat|
|Calculated MW||36943 Da|
|Homology||Rat, mouse - 13/15 amino acid residues identical.|
|Other Names||Melanocortin receptor 4, MC4-R, MC4R|
|Related products for control experiments||Control peptide antigen (supplied with the antibody free of charge).|
|Target/Specificity||Peptide (C)HRGMHTSLHLWNRSS, corresponding to amino acid residues 6-20 of human MC4R (Accession P32245 ). Extracellular, N terminal.|
|Peptide Confirmation||Confirmed by mass-spectrography analysis.|
|Application Details||Immunocytochemistry (IC): - Mouse hippocampal neurons (see Shen, Y. et al. (2013) in Product Citations).|
|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.|
|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.|
|Formulation||Lyophilized powder. Phosphate buffered saline (PBS), pH 7.4, 1% BSA, 0.025% NaN3.|
Thousands of laboratories across the world have published research that depended on the performance of antibodies from Abgent to advance their research. Check out links to articles that cite our products in major peer-reviewed journals, organized by research category.
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Provided below are standard protocols that you may find useful for product applications.
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.
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.
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