ライフサイエンスコーパス: gamma MSH

1 eptide gamma-melanocyte-stimulating hormone (gamma-MSH).

2 systemic or local administration of [D-Trp8]-gamma-MSH.

3 consequence of impaired POMC processing into gamma-MSH.

4 elanocortin prohormone: ACTH, alpha-MSH, and gamma-MSH.

5 the anti-inflammatory effects of [d-Trp(8)]-gamma-MSH.

6 Intravenous infusion of gamma-MSH (0.2 pmol/min) for 30 min to PC2(-/-) mice aft

7 The effects of gamma-MSH (1.25 nmol) are not inhibited by the intracaro

8 In wild-type (WT) macrophages, [D-Trp8]-gamma-MSH activated MC3-R (as tested by accumulation of

9 ve systematically designed a group of linear gamma-MSH analogues and evaluated their biological activ

10 rg-Trp in gamma-MSH, two different series of gamma-MSH analogues have been designed and synthesized a

11 involved in ligand-receptor interaction for gamma-MSH analogues that may explain the enhanced bindin

12 A number of novel cyclic truncated gamma-MSH analogues were designed and synthesized, in wh

13 gamma-MSH and ACTH(4-10), but not alpha-MSH, elicit dose

14 the structurally related agonists alpha-MSH, gamma-MSH, and Ac-Nle4-cyclic-[Asp5,His6,D-Phe7,Arg8,Trp

15 urate crystals was attenuated by [d-Trp(8)]-gamma-MSH, and this effect was prevented by synthetic [A

16 It was found that cyclization of the native gamma-MSH around the highly conserved sequence can lead

17 Using gamma-MSH as a template, we developed a peptide, [Leu(3)

18 cell surface, and cleaves its substrate, pro-gamma-MSH, at a specific bond.

19 Administration of an MC(3) agonist, D[Trp8]-gamma-MSH, attenuated disease incidence and severity in

20 o a markedly hypertensive level while plasma gamma-MSH concentration remained severely depressed.

21 gamma-MSH deficiency results in marked salt-sensitive hy

22 cyclic gamma-melanocyte-stimulating hormone (gamma-MSH)-derived hMC3R/hMC5R antagonists.

23 We also demonstrate here that [d-Trp(8)]-gamma-MSH displays a dual mechanism of action by inducin

24 ent of the selective MC3R agonist [d-Trp(8)]-gamma-MSH for the treatment of inflammatory pathologies,

25 gamma-MSH (gamma-melanocyte-stimulating hormone, H-Tyr-V

26 A series of cyclic lactam analogues of gamma-MSH (H-Tyr1-Val2-Met3-Gly4-His5-Phe6-Arg7-Trp8-Asp

27 very important for selectivity of alpha-MSH/gamma-MSH hybrids for hMCRs.

28 Thus, the key residues of gamma-MSH identified in this study include the aromatic

29 id not alter MAP versus LSD mice, but plasma gamma-MSH immunoreactivity was more than double the LSD

30 ion accompanied by elevated plasma levels of gamma-MSH; infusion of exogenous gamma-MSH to these mice

31 Systemic treatment of mice with [d-Trp(8)]-gamma-MSH inhibited KC release and polymorphonuclear cel

32 Injection of 60 fmol of gamma-MSH into the lateral cerebral ventricle of hyperte

33 Administration of a stable analogue of gamma-MSH intra-abdominally by microosmotic pump to PC2(

34 0 pmol) hypotension and bradycardia, whereas gamma-MSH is less effective.

35 t that PC2-dependent processing of POMC into gamma-MSH is necessary for the normal response to the HS

36 The gamma-melanocyte-stimulating hormone (gamma-MSH) is a natriuretic peptide derived from the N-t

37 t, also known as pro-gamma-melanotropin (pro-gamma-MSH), is required, releasing shorter fragments tha

38 recessive yellow (e/e) mice with [d-Trp(8)]-gamma-MSH led to accumulation of cAMP, indicating MC3R r

39 he enhanced binding affinities of the Nle(3)-gamma-MSH-NH(2) analogues.

40 ith d-Nal(2')(8) and Phe(6) with d-Phe(6) in gamma-MSH-NH(2) forms a selective antagonist for the hMC

41 with Pro(5) and Trp(8) with d-Nal(2')(8) in gamma-MSH-NH(2) leads to a highly potent and selective a

42 pharmacophores of MTII, SHU9119, and Ac-NDP-gamma-MSH-NH(2) replaced by Pro or trans-/cis-4-guanidin

43 2')(6) and replacing Trp(8) with d-Trp(8) at gamma-MSH-NH(2) yields a selective partial agonist for t

44 ing showed that, at the C-terminal of Nle(3)-gamma-MSH-NH(2), there is a reverse-turn-like structure,

45 eveloped a peptide, [Leu(3), Leu(7), Phe(8)]-gamma-MSH-NH2 (compound 5), which is 16-fold selective f

46 [Leu(3), Leu(7), Phe(8)]-gamma-MSH-NH2 is ideal for inducing short-term skin pigm

47 -/-)), necessary for processing of POMC into gamma-MSH, or the melanocortin receptor 3 gene (Mc3r(-/-

48 Absence of Mc3r produces gamma-MSH resistance and hypertension on the HSD.

49 d-2-naphthylalanine (d-Nal(2')) scan of the gamma-MSH sequence at position 6 and 8 and the replaceme

50 equential replacement of each residue in the gamma-MSH sequence with the corresponding D-isomer resul

51 The native gamma-MSH shows weak binding at all three receptors (i.e

52 vivo, administration of 3-30 microg [D-Trp8]-gamma-MSH significantly inhibited leukocyte influx and c

53 sion that is rapidly improved with exogenous gamma-MSH through a central site of action.

54 s found that changing the C-terminal acid in gamma-MSH to an amide and replacing Met with Nle leads t

55 a levels of gamma-MSH; infusion of exogenous gamma-MSH to these mice had no effect on MAP.

56 tion of the pharmacophore His-Phe-Arg-Trp in gamma-MSH, two different series of gamma-MSH analogues h

57 ng, we have engineered peptides by cyclizing gamma-MSH using a thioether bridge.

58 rtin type 3 receptor (MC3-R) ligand [D-Trp8]-gamma-MSH, validating in vitro results with analyses in

59 t greater than in wild-type mice, but plasma gamma-MSH was reduced to one-seventh the wild-type value

60 tribute to the 3D topographical structure of gamma-MSH, we have systematically designed a group of li

61 evented the inhibitory actions of [d-Trp(8)]-gamma-MSH, whereas HS024 was inactive.

62 mediated pressor and tachycardic actions of gamma-MSH, which, likely, are mediated by an as yet unid