Proopiomelanocortin (POMC) is a pro-peptide and multifunctional precursor protein for melanocyte-stimulating hormone (MSH) and adrenocorticotropic hormone ACTH. The POMC gene is mapped to human chromosome 2p23.3. It is expressed in skin, pituitary gland, and tissues of the immune system.
Immunogen
Peptide with sequence C-NAIIKNAYKKGE from the C Terminus of the protein sequence according to NP_000930.1; NP_001030333.1.
Biochem/physiol Actions
Proopiomelanocortin (POMC) expression is regulated by hypermethylation of the upstream CpG-rich island in the gene. Mutations in the POMC gene are implicated in adrenocorticotropic hormone (ACTH) deficiency. Adrenal insufficiency and obesity are correlated to loss of function mutations in POMC.
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Physical form
Supplied at 0.5 mg/mL in Tris saline with 0.02% sodium azide and 0.5% bovine serum albumin.
Disclaimer
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
Proopiomelanocortin (POMC)-derived peptides such as melanocortins and β-endorphin (β-ED) exert their pleiotropic effects via binding to melanocortin receptors (MCR) and opioid receptors (OR). There is now compelling evidence for the existence of a functional POMC system within the osteoarticular system.
International journal of pediatric endocrinology, 2011(1), 5-5 (2011-08-24)
Isolated hypocortisolism due to ACTH deficiency is a rare condition that can be caused by homozygous or compound heterozygous mutations in the gene encoding proopiomelanocortin (POMC). Loss of function mutations of POMC gene typically results in adrenal insufficiency, obesity and
Overeating leads to obesity, a low-grade inflammatory condition involving interleukin-17A (IL-17A). While pro-opiomelanocortin (POMC) neurons regulate feeding, their connection with IL-17A is not well understood. To impair IL-17A signaling in POMC neurons, IL-17A receptor (Il17ra) was deleted by crossing IL17ra-flox
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