ライフサイエンスコーパス: alphaMSH

1 ion of alpha melanocyte stimulating hormone (alphaMSH).

2 n and was entirely due to an increase in Act-alphaMSH.

3 by a dramatically increased stability of Act-alphaMSH.

4 ding to increased hypothalamic levels of Act-alphaMSH.

5 signaling protein, endogenous inhibitors of alphaMSH.

6 the pro-opiomelanocortin (POMC) precursor of alphaMSH.

7 tion of POMC neurons or central injection of alphaMSH, a product of POMC, is abolished in obese mice.

8 e higher biological activity of N-acetylated alphaMSH (Act-alphaMSH) compared with that of N-desacety

9 n their sensitivity to, and requirement for, alphaMSH agonist.

10 iated activation of GIRK channels, while the alphaMSH analog, MTII, had no effect on activity of NPY

11 alogue of alpha MSH, [125I] Nle(4), D-Phe(7)-alphaMSH and unlabeled MCH.

12 nists, alpha melanocyte stimulating hormone (alphaMSH) and interleukin-1 receptor antagonist (IL-1ra)

13 ced by alpha-melanocyte-stimulating hormone (alphaMSH) and melanin-concentrating hormone (MCH).

14 nostaining revealed that alpha-melanocortin (alphaMSH) and neuropeptide Y (NPY) accumulated below the

15 pigment-related genes targeted by ASP and by alphaMSH, and provide insights into the pleiotropic mole

16 NPY and alphaMSH are expressed in distinct neurons in the arcuat

17 We suggest that NEI/alphaMSH autoantibodies may interfere with the fine regu

18 did not compete with [125I] Nle(4), D-Phe(7)-alphaMSH binding.

19 nd body weight were correlated negatively to alphaMSH, but not NPY in PVN.

20 gical activity of N-acetylated alphaMSH (Act-alphaMSH) compared with that of N-desacetylated alphaMSH

21 e arcuate nucleus of the hypothalamus, where alphaMSH decreases and NPY increases food intake and bod

22 Comparison of the phenotypes of alphaMSH-deficient mice and humans in conjunction with t

23 haMSH) compared with that of N-desacetylated alphaMSH (Des-alphaMSH) is unclear, and regulation of ac

24 AgRP-neurons, the anorexigenic neuropeptide alphaMSH for POMC-neurons, and two growth-stimulatory pe

25 and alpha-melanocortin stimulating hormone (alphaMSH)-immunoreactive fibers were significantly reduc

26 or, Act-alphaMSH is far more potent than Des-alphaMSH in stimulating cAMP accumulation, an effect cau

27 istence of NPY signalling is blunted by high alphaMSH in the fed state, while alphaMSH signalling is

28 to fibronectin was significantly reduced by alphaMSH in the wild type transfectants whereas this was

29 ones; binding to laminin was not affected by alphaMSH in this cell line.

30 At similar MC1 receptor numbers per cell, alphaMSH increased intracellular cAMP in wild type MC1R

31 timuli alpha-melanocyte stimulating hormone (alphaMSH) increases STIM1 mRNA and protein levels.

32 ergy balance in unstressed rats, possibly by alphaMSH input to PVN, and that ARC also is necessary fo

33 Neonatal leptin treatment neither rescued alphaMSH inputs onto neuroendocrine neurons, nor altered

34 expressing the melanocortin 4 receptor, Act-alphaMSH is far more potent than Des-alphaMSH in stimula

35 Moreover, Des-alphaMSH is rapidly degraded in the hypothalamus after i

36 eptide alpha-melanocyte-stimulating hormone (alphaMSH) is a melanocortin 4 receptor agonist, and its

37 d with that of N-desacetylated alphaMSH (Des-alphaMSH) is unclear, and regulation of acetylation by l

38 We show here that total hypothalamic alphaMSH levels are decreased in leptin-deficient ob/ob

39 lity, this posttranslational modification of alphaMSH may play a critical role in leptin action via t

40 ted by alpha-melanocyte stimulating hormone (alphaMSH), MC1R function can be antagonized by a secrete

41 We show that downstream of alphaMSH, microphthalmia-associated transcription factor

42 The increase in total alphaMSH occurred as soon as 3 h after leptin injection

43 ariants could alter the autocrine effects of alphaMSH on melanoma cell behaviour, thereby affecting e

44 rine melan-a melanocytes treated with ASP or alphaMSH over a 4-day time course using genome-wide olig

45 NA and alpha-melanocyte-stimulating hormone (alphaMSH) peptide levels were markedly reduced in POMC-S

46 After release, NPY and alphaMSH peptides compete to control cAMP-the amplitude

47 ne/alpha-melanocyte-stimulating hormone (NEI/alphaMSH) peptides.

48 ns is associated with variant alleles of the alphaMSH receptor gene, MC1R.

49 This was accompanied by diminished levels of alphaMSH receptor, MC4R, in kisspeptin neurons.

50 Mammals have five alphaMSH receptors (melanocortin receptors) and one or t

51 this competition by simultaneously elevating alphaMSH release and suppressing NPY release(7,8), there

52 ted by high alphaMSH in the fed state, while alphaMSH signalling is blunted by high NPY in the fasted

53 In growth inhibition experiments, alphaMSH significantly reduced growth of wild type MC1R

54 Further, alphaMSH stimulates STIM1 promoter-driven luciferase act

55 elease alpha-melanocyte stimulating hormone (alphaMSH, the ligand for MC1R), therefore MC1R variants

56 romoting POMC axons release the neuropeptide alphaMSH to increase cAMP.