ライフサイエンスコーパス: gamma-MSH

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

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

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

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

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

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

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

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

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

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

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

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

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

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

15 2')(6) and replacing Trp(8) with d-Trp(8) at gamma-MSH-NH(2) yields a selective partial agonist for t

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

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

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

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

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

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

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

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

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

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

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

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

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

29 consequence of impaired POMC processing into gamma-MSH.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

61 0 pmol) hypotension and bradycardia, whereas gamma-MSH is less effective.