neuromedin u, rat

Neuromedin U,a 23-amino acid brain-gut peptide, regulates several important physiological functions through its cognate receptor NMUR2 in the central nervous system, including energy balance, stress response, and nociception.

Neuromedin U, rat acetate is a 23-amino acid brain-gut peptide. Neuromedin U (NMU), through its cognate receptor NMUR2 in the central nervous system, regulates several important physiological functions, including energy balance, stress response, and nociception.

Neuromedin U (rat TFA), a 23-amino acid brain-gut peptide, operates via its specific receptor NMUR2 in the central nervous system to modulate critical physiological processes such as energy homeostasis, stress response, and nociception.

Neuromedin U, rat TFA is a 23-amino acid brain-gut peptide.

Neuromedin S(rat) TFA, a 34-amino acid peptide derivative of rat Neuromedin S, is a neuropeptide sourced from the rat brain that functions as a ligand for the G protein-coupled receptor FM4/TGR-1 [1].

Neuromedin U-25 (porcine) is a peptide known for its uterotonic and hypertensive properties [1].

Potent, endogenous neuromedin U receptor agonist (EC50 values are 65 and 91 pM at NMU1 and NMU2 respectively). Induces phase shifts in the circadian rhythm of locomotor activity following i.c.v. administration. Potent endogenous anorexigenic peptide.

Neuromedin U (NMU) is a neuropeptide first demonstrated to drive smooth muscle contraction.1Translated as a 174 amino acid propeptide, NMU is cleaved to different lengths in different animals. It has diverse receptor-mediated rolesin vivo, as it regulates feeding, vasoconstriction, nociception, and bone remodeling and contributes to obesity, cancer and septic shock.2,2NMU-25 is the active form of NMU in humans. It binds with high affinity to receptors on human left ventricle and coronary artery (KDs = 0.26 and 0.11 nM, respectively), eliciting endothelium-independent vasoconstriction.3NMU-25 also suppresses glucose-stimulated insulin secretion in human islets, and this effect is lost in NMU R165W mutants, resulting in early-onset obesity.4 1.Mitchell, J.D., Maguire, J.J., and Davenport, A.P.Emerging pharmacology and physiology of neuromedin U and the structurally related peptide neuromedin SBritish Journal of Pharmacology15887-103(2009) 2.Greenwood, H.C., Bloom, S.R., and Murphy, K.G.Peptides and their potential role in the treatment of diabetes and obesityRev.Diabet.Stud.8(3)355-368(2011) 3.Mitchell, J.D., Maguire, J.J., Kuc, R.E., et al.Expression and vasoconstrictor function of anorexigenic peptides neuromedin U-25 and S in the human cardiovascular systemCardiovascular Research81353-361(2009) 4.Alfa, R.W., Park, S., Skelly, K.R., et al.Suppression of insulin production and secretion by a decretin hormoneCell Metabolism21(2)323-333(2015)