Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

By comparing the results of energy calculation for alpha-MSH and its semirigid analogues Ac-[ Cys4 , Cys10 ]-alpha- MSH4 -10-NH2, Ac-[ Cys4 , Cys10 ]-alpha- MSH4 -13-NH2, and [ Cys4 - Cys10 ]-alpha-MSH, a detailed description of two possible bioactive conformations for the 'specific' central site of alpha- MSH6 -9 is proposed representing variants of chain-reversal structure. A possible explanation of the rise in melanotropic activity of the latter two semirigid analogues is presented.
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PMID:Possible bioactive conformations of alpha-melanotropin. 672 68

Analogues of a melanocyte-stimulating hormone (alpha-MSH) have been documented to be effective in inducing integumental melanogenesis in several species. These melanotropin analogues are more potent than the natural hormone and have prolonged biological activity, without apparent teratogenic or other toxic effects, at least in rodents. In a pilot study, a cyclic alpha-MSH analogue, Ac-[Nle4, Asp5, D-Phe7, Lys10] alpha-MSH4-10-NH2, was administered SC to a dog at a dose of 1 mg of analogue in 1 ml of 0.9% NaCl for 3 weeks, without noticeable adverse effects. There was gradual and extensive darkening of the coat, which originally was predominantly tan, with tips of black. Initially, the darkening involved face and extremities, then gradually expanded to include the trunk and tail hair. Visual pigmentation peaked approximately 2 months after injections were completed. As new hair growth continued subsequent to the injections, the original tan color appeared at the proximal end of the hair shaft, leaving a dark terminal band on all affected hairs. These observations clearly indicated that follicular melanogenesis can be induced in dogs by treatment with a melanotropic peptide.
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PMID:Coat color darkening in a dog in response to a potent melanotropic peptide. 787 84

Binding and stimulation of cAMP by the melanotropin peptides alpha-MSH (alpha-melanocyte-stimulating hormone) and its superpotent analogues [Nle4, DPhe7]alpha-MSH (MT-I) and Ac-[Nle4,[formula: see text]alpha-MSH4-10-NH2 (MT-II) were undertaken to examine their respective properties on the human peripheral melanocyte melanocortin receptor, hMC1R. alpha-MSH was found to possess a binding IC50 value of 6.5 +/- 0.9 x 10(-9) M and cAMP EC50 value of 2.0 +/- 0.6 x 10(-9) M. MT-I possesses a binding IC50 value of 1.2 +/- 0.3 x 10(-9) M and a cAMP EC50 of 0.5 +/- 0.03 x 10(-9) M. MT-II possesses a binding IC50 of 0.57 +/- 0.08 x 10(-9) M and cAMP EC50 value of 0.20 +/- 0.05 x 10(-9) M.
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PMID:Binding and cAMP studies of melanotropin peptides with the cloned human peripheral melanocortin receptor, hMC1R. 798 May 88

The existence of multiple brain melanocortin receptor types has been postulated, based on the complex pharmacology of intracerebrally administered melanocortin (melanocyte-stimulating hormone-related) peptides. In this study, this hypothesis was tested by determining whether different brain melanocortin receptor populations can be discriminated on a pharmacologic or neuroanatomic basis. The abilities of various pharmacologically active native melanocortins and structural analogs, as well as other test substances, to compete with biologically active [125I]Nle4,D-Phe7-alpha-MSH ([125I]NDP-MSH) for binding to melanocortin receptors was determined, by in vitro binding and autoradiography in frozen rat brain tissue sections. We have previously shown that native melanocortins including alpha-MSH, gamma-MSH and ACTH1-39 compete with [125I]NDP-MSH for binding to brain tissue sites. In the present studies, each of the melanocortin peptides alpha-MSH, des-acetyl-alpha-MSH, beta-MSH and ACTH1-24 when present at 1 microM virtually eliminated [125I]NDP-MSH binding in each of a series of brain structures, including medial preoptic area, caudate putamen, olfactory tubercle, bed nucleus of the stria terminalis, ventral part of the lateral septal nucleus, hypothalamic periventricular and paraventricular nuclei, dorsal anterior amygdaloid area, substantia innominata and thalamic paraventricular nucleus; as well as in extraorbital lacrimal gland, a peripheral melanocortin target. In contrast, the behaviorally and neurotrophically active melanocortin analogs Met(O2),D-Lys,Phe9-alpha-MSH4-9 (Org2766), ACTH4-9, and the antipyretic peptide alpha-MSH11-13 did not affect [125I]NDP-MSH binding at concentrations up to 100 microM, implying that the receptors or receptor binding sites which mediate the actions of these analogs must comprise additional types, distinct from those which bind [125I]NDP-MSH. Binding of [125I]NDP-MSH was also unaffected by the nonmelanotropic peptides ACTH1-4, ACTH34-39 and vasoactive intestinal polypeptide (VIP) and by the antipyretic drugs acetaminophen and lysine-salicylate. Although some of the brain structures are known to express mRNA encoding a gamma-MSH-preferring melanocortin receptor type known as MC3, the relative order of binding affinities of melanocortins, determined in concentration-response studies, was NDP-MSH > or = ACTH1-24 > or = alpha-MSH > gamma-MSH > ACTH4-10 in all brain structures. This suggests that other melanocortin receptor type(s) in addition to MC3 probably account for most of the [125I]NDP-MSH binding detectable in the brain.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Heterogeneity of brain melanocortin receptors suggested by differential ligand binding in situ. 817 50

The thermoregulatory effects of alpha-melanocyte stimulating hormone (MSH), its potent analog, [Nle4,D-Phe7]-alpha-MSH (NDP-MSH), and the 1-7, 4-10, and 7-13 amino acid fragments of NDP-MSH were examined by administering these substances to the anterior hypothalamic-preoptic area (AHPOA) of rats. In Experiments 1a (MSH) and 1b (NDP-MSH), animals received 0, 0.5, 1, 5, 10, or 50 pM peptide in 0.5 microliters sterile saline (n = 6/group), with core rectal temperatures being recorded 0, 10, 20, 30, 40, 50, and 60 min after injection. In Experiment 2, subjects received 5 pM NDP-MSH1-7, NDP-MSH4-10, NDP-MSH7-13, NDP-MSH, or the vehicle, 0.5 microliters sterile saline, in a counterbalanced fashion (n = 13). Results indicated a significant effect of dose for both MSH, F(5, 30) = 2.81, p = 0.03, and NDP-MSH, F(5, 30) = 4.98, p = 0.002. A Newman-Keul's analysis indicated that mean temperatures for all groups receiving MSH or NDP-MSH were significantly greater than for the group that received saline (p < 0.05). An analysis of the data from Experiment 2 indicated a significant effect of substance, F(4, 48) = 17.31, p < 0.001. Mean temperature of animals receiving NDP-MSH, the 4-10, or the 7-13 fragments, did not differ from each other but were significantly greater than mean temperatures for animals receiving sterile saline or the 1-7 fragment of NDP-MSH (p < 0.05).
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PMID:Alpha-melanocyte-stimulating hormone (MSH) and [Nle4,D-Phe7]-alpha-MSH: effects on core temperature in rats. 838 52

The injection of alpha-MSH or of one of its analogues ([Nle4-D.Phe7] alpha-MSH4-10) reduced, in vivo, the release of two cytokines (IL-1 alpha and TNF alpha) involved in inflammation. The inflammatory state was induced in BALB/c mice by intraperitoneal injection of a sublethal dose of lipopolysaccharides (LPS). The assay of these cytokines by ELISA showed a reduction of 20% with alpha-MSH and between 30 and 60% with the alpha-MSH analogue. The alpha-MSH or the analogue was administered in one of two ways: intravenously or subcutaneously. The most efficient method seemed to be the subcutaneous one because it improved the activity 10,000 times more than the intravenous method. Moreover, the analogue induced a regression of mortality in the animals treated by the intravenous method. Our results show that alpha-MSH and one of its analogues inhibit IL-1 alpha and TNF alpha, and can be used as anti-inflammatory molecules.
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PMID:The administration of an alpha-MSH analogue reduces the serum release of IL-1 alpha and TNF alpha induced by the injection of a sublethal dose of lipopolysaccharides in the BALB/c mouse. 888 14


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