ライフサイエンスコーパス: alpha-MSH

1 alpha-MSH also increased circulating levels of free thyr

2 alpha-MSH and other bioactive peptides are cleavage prod

3 alpha-MSH at physiologic doses potently suppressed basop

4 alpha-MSH decreased 64% in ARC and 29% in mPVN (P < 0.05

5 alpha-MSH decreased intra-abdominal fat and markedly enh

6 alpha-MSH induces Fos expression in supraoptic oxytocin

7 alpha-MSH infused at the same rate had no effect on MAP,

8 alpha-MSH is a potent agonist at hMC4R but not at hMC2R.

9 alpha-MSH modulated the excitatory-inhibitory balance in

10 alpha-MSH preserves GAD67 expression and prevents loss o

11 alpha-MSH protects against both kidney and lung damage a

12 alpha-MSH signaling strongly induces PGC-1alpha expressi

13 alpha-MSH signals by binding to the melanocortin-1 recep

14 alpha-MSH was also capable of reducing peroxide accumula

15 alpha-MSH, L-Lys-L-Pro-L-Val, and L-Lys-L-Pro-D-Val all

16 alpha-MSH, melanotan II (MTII), and selective MC3R or MC

17 thetic [Ac-Nle(4)-c[Asp(5)-2'-Nal(7),Lys(10)]alpha-MSH(4-10)-NH(2) (SHU9119)] and natural [agouti-rel

18 etic acid]-ReO-[Cys(3,4,10),d-Phe(7),Arg(11)]alpha-MSH(3-13) ((212)Pb-DOTA-Re(Arg(11))CCMSH) cured 45

19 SH peptide, ReO[Cys(3,4,10),d-Phe(7),Arg(11)]alpha-MSH(3-13) (ReCCMSH(Arg(11))), has shown high in vi

20 [Cys(3,4,10),d-Phe(7),Arg(11)]alpha-MSH(3-13) [(Arg(11))CCMSH] and [1,4,7,10-tetraazac

21 D-Lys-ReCCMSH(Arg(11)), and [Nle(4),D-Phe(7)]alpha-MSH (NDP) (for comparison), labeled with N-succini

22 receptor-binding peptides, [Nle(4),D-Phe(7)]alpha-MSH (NDP), as a linear peptide standard.

23 ) coupled ReO-cyclized [Cys(3,4,10),D-Phe(7)]alpha-MSH(3-13) (DOTA-ReCCMSH).

24 ting metallopeptide ReO[Cys(3,4,10),D-Phe(7)]alpha-MSH(3-13) (ReCCMSH) was shown to possess high tumo

25 e bond cyclization, DOTA-[Cys(4,10),D-Phe(7)]alpha-MSH(4-13) (CMSH).

26 cells and (125)I-(Tyr(2))-[Nle(4),D-Phe(7)]-alpha-MSH [(125)I-(Tyr(2))-NDP] as a radioligand.

27 Since there is little know about alpha-MSH as an anti-apoptotic factor, the effects of al

28 study first showed that in the DMH abundant alpha-MSH and agouti-related protein fibers are in close

29 onstrated that in-vitro-generated des-acetyl alpha-MSH successfully activated the melanocortin 4 rece

30 e H2O2-mediated oxidation of epidermal ACTH, alpha-MSH, and beta-endorphin in vitiligo owing to oxida

31 cAMP, albeit with a lower potency than ACTH, alpha-MSH, and beta-MSH.

32 In addition, alpha-MSH did not improve mitochondrial membrane potenti

33 In addition, alpha-MSH promotes survival of the alternatively activat

34 In addition, alpha-MSH reduced gastric tone and mean arterial blood p

35 mino terminus of one of the highest-affinity alpha-MSH receptor-binding peptides, [Nle(4),D-Phe(7)]al

36 and altered anxiety that were rescued after alpha-MSH treatment.

37 on of the receptor by the endogenous agonist alpha-MSH.

38 gnificantly, treatment with the MC1R agonist alpha-MSH or activation of the stress response kinase p3

39 It is regulated by internal agonist (alpha-MSH) and antagonists (Agouti).

40 surface that were responsive to the agonist, alpha-MSH, by 75%.

41 functionality using the endogenous agonists alpha-MSH, beta-MSH, gamma2-MSH, ACTH(1-24), the antagon

42 re potent than the other endogenous agonists alpha-MSH, gamma2-MSH, ACTH(1-24).

43 ons of the hMC2R did not significantly alter alpha-MSH binding affinity and potency except substituti

44 In this study, an alpha-MSH analog, Ac-Nle-Asp-His-D-Phe-Arg-Trp-Gly-Lys-N

45 ore, a negative correlation between OX-A and alpha-MSH serum levels was found in obese mice as well a

46 LPXRFa-R are expressed only in LH, ACTH, and alpha-MSH cells.

47 g MC4R vary in their sensitivity to Agrp and alpha-MSH with regard to their effect on feeding.

48 ro-TRH mRNA-containing neurons and CART- and alpha-MSH-immunoreactive (IR) axons.

49 ation of cathepsin L with beta-endorphin and alpha-MSH in the intermediate pituitary and with ACTH in

50 the production of ACTH, beta-endorphin, and alpha-MSH peptide hormones in the regulated secretory pa

51 major decreases in ACTH, beta-endorphin, and alpha-MSH that were reduced to 23, 18, and 7% of wild-ty

52 Microinjection of the agonists (MT-II and alpha-MSH) into the overlying nucleus of the solitary tr

53 in, bradykinin, angiotensins II and III, and alpha-MSH, suggesting its role in the processing of tiss

54 and that expression of the receptor mRNA and alpha-MSH sensitivity are both stimulated by leptin.

55 pression in supraoptic oxytocin neurons, and alpha-MSH melanocortin-4 receptors (MC4Rs) are highly ex

56 mologous regions of hMC2R were performed and alpha-MSH binding and signaling were examined.

57 follicle melanocytes secreted both POMC and alpha-MSH, and this was enhanced in response to corticot

58 ained significantly more ACTH than POMC, and alpha-MSH was detected only in keratinocytes.

59 studied the expression of MC1R under UVR and alpha-MSH stimulation in skin of different ethnic origin

60 ed the potential contribution of NPY/Y1R and alpha-MSH/MC3/4R-signaling to accumbens-induced high-fat

61 regulatory activity was neutralized by anti-alpha-MSH antibodies.

62 0 nM), the analogue obtained is as potent as alpha-MSH in the frog skin MC1R assay.

63 Therefore, as alpha-MSH promotes the alternative activation of macroph

64 a imaging and potential radiotherapy because alpha-MSH receptors are overexpressed on both mouse and

65 n-based ligand Phe(7) by differences between alpha-MSH and NDP-MSH agonist potencies.

66 wed that intravenously injected biotinylated alpha-MSH phage were retained within melanoma tumors at

67 way, while AgRP binds competitively to block alpha-MSH binding and blocks the constitutive activity m

68 Although ASIP and HBD3 each blocked alpha-MSH-mediated induction of the signaling pathway, o

69 is, hyperphagia, and weight gain by blunting alpha-MSH production via CB1R-induced and extracellular-

70 Nevertheless, both alpha-MSH doses effectively inhibited LPS-induced periph

71 sing beta-amyloid peptide load in the brain, alpha-MSH improves spatial memory in TgCRND8 mice and pr

72 ase, TRP-1, and TRP-2 were not influenced by alpha-MSH.

73 ->PVH satiety circuit, and its modulation by alpha-MSH, provides insight into regulation of hunger an

74 ricular nucleus of the hypothalamus (PVN) by alpha-MSH and AgRP can be mediated independently of Galp

75 ate that the diminution in TUNEL staining by alpha-MSH is through alpha-MSH mediating suppression of

76 hat both ETA and ETB are capable of cleaving alpha-MSH.

77 The DOTA-conjugated alpha-MSH analogs were radiolabeled with (111)In and exa

78 are innervated by axon terminals containing alpha-MSH.

79 were contacted by axon terminals containing alpha-MSH.

80 A novel cyclic alpha-MSH peptide, 1,4,7,10-tetraazacyclododecane-1,4,7,

81 library consists of a novel series of cyclic alpha-MSH analogues that have disulfide bridges between

82 a novel radiolabeled lactam bridge-cyclized alpha-MSH peptide for melanoma imaging and treatment.

83 A transition metal rhenium-cyclized alpha-MSH peptide, ReO[Cys(3,4,10),d-Phe(7),Arg(11)]alph

84 rticotropin to alpha-MSH, thereby decreasing alpha-MSH peptide production.

85 elanotan-2, an analog of the POMC derivative alpha-MSH, suppressed adult obesity in Gpr45 mutants.

86 se of the other closely related (111)In-DOTA-alpha-MSH conjugates.

87 nsgenic littermates were treated with either alpha-MSH or vehicle via daily intraperitoneal injection

88 icantly inhibited by coinjection with excess alpha-MSH peptide (P < 0.05), indicating that (18)F-FB-N

89 gical MC4-R blockade during fever, exogenous alpha-MSH can exacerbate fever, probably by acting via o

90 g-recognized antipyretic effect of exogenous alpha-MSH is mediated by the melanocortin-4 receptor (MC

91 uction of the potent immunomodulating factor alpha-MSH by TCR-stimulated primed T cells through which

92 nal tail, I316S, showed reduced affinity for alpha-MSH but retained normal affinity for the antagonis

93 residues in TMs of the hMC4R are crucial for alpha-MSH binding and signaling.

94 ntation, and a role has been put forward for alpha-MSH as an effective antioxidant.

95 -NAPamide is a promising molecular probe for alpha-MSH receptor-positive melanoma PET and warrants fu

96 he absence of expression of the receptor for alpha-MSH (MC1-R), as assessed by Northern blot analysis

97 alpha-MSH and expression of the receptor for alpha-MSH (MC1-R).

98 M3, and TM6 of the hMC4R are responsible for alpha-MSH binding and signaling.

99 ecular determinants of hMC4R responsible for alpha-MSH binding and signaling.

100 Furthermore, alpha-MSH and AgRP-ir somata and fibers are pronounced a

101 show for the first time that a peptide, here alpha-MSH, can induce differential regulation of dendrit

102 of the alpha-melanocyte-stimulating hormone (alpha-MSH) analog 1,4,7,10-tetraazacyclododecane-1,4,7,1

103 enated alpha-melanocyte-stimulating hormone (alpha-MSH) analogs were proposed for melanoma imaging an

104 of new alpha-melanocyte-stimulating hormone (alpha-MSH) analogues which are N-terminal modified with

105 gands, alpha melanocyte stimulating hormone (alpha-MSH) and agouti-related peptide (AGRP), on feeding

106 uch as alpha-melanocyte-stimulating hormone (alpha-MSH) and anorexigenic neurotransmitter serotonin.

107 binds alpha-melanocyte-stimulating hormone (alpha-MSH) and has a central role in the regulation of a

108 cludes alpha-melanocyte-stimulating hormone (alpha-MSH) and its endogenous antagonist, agouti-related

109 igenic alpha-melanocyte stimulating hormone (alpha-MSH) and orexigenic Agouti-related protein (AgRP)

110 ptides alpha-melanocyte stimulating hormone (alpha-MSH) and oxytocin, when administered centrally, pr

111 gonist alpha-melanocyte-stimulating hormone (alpha-MSH) and the orexigenic antagonist agouti-related

112 onist, alpha-melanocyte-stimulating hormone (alpha-MSH) and to an antagonist/inverse agonist, agouti-

113 n, and alpha-melanocyte stimulating hormone (alpha-MSH) are synthesized by proteolytic processing of

114 d with alpha melanocyte stimulating hormone (alpha-MSH) as well as neuropeptide Y (NPY).

115 eptide alpha-melanocyte stimulating hormone (alpha-MSH) attenuates GABAergic loss and thus improves c

116 for alpha-melanocortin-stimulating hormone (alpha-MSH) binding, in this study, we utilized both rece

117 ase of alpha-melanocyte-stimulating hormone (alpha-MSH) from ex vivo hypothalamic explants.

118 Alpha-melanocyte stimulating hormone (alpha-MSH) has pigmentary, anti-inflammatory, antipyreti

119 s with alpha-melanocyte stimulating hormone (alpha-MSH) in the arcuate nucleus neurons and we have re

120 es and alpha-melanocyte stimulating hormone (alpha-MSH) in the paraventricular nucleus (PVN) were exa

121 PY and alpha-melanocyte-stimulating hormone (alpha-MSH) inhibit and stimulate, respectively, PVN-RVLM

122 alpha-Melanocyte stimulating hormone (alpha-MSH) is a neuropeptide that suppresses host inflam

123 Alpha-melanocyte-stimulating hormone (alpha-MSH) is an antiinflammatory cytokine, which inhibi

124 eptide alpha-melanocyte stimulating hormone (alpha-MSH) is an important regulator of immune cell acti

125 Alpha-melanocyte stimulating hormone (alpha-MSH) is one of the known endogenous agonists for t

126 eptide alpha-melanocyte-stimulating hormone (alpha-MSH) is reduced, yet the mRNA of its precursor pro

127 es and alpha-melanocyte-stimulating hormone (alpha-MSH) of pars intermedia melanotropes, provides a u

128 ole of alpha-melanocyte-stimulating hormone (alpha-MSH) on basophil function.

129 report that melanocyte-stimulating hormone (alpha-MSH) or ACTH induce ATR-pS435, enhance XPA's assoc

130 uch as alpha-melanocyte-stimulating hormone (alpha-MSH) or antagonists such as agouti-related protein

131 ies of alpha-melanocyte-stimulating hormone (alpha-MSH) peptide analogs.

132 abeled alpha-melanocyte stimulating hormone (alpha-MSH) peptide analogues: 125I-(Tyr2)-[Nle4, D-Phe7]

133 clized alpha-melanocyte-stimulating hormone (alpha-MSH) peptide on its melanoma-targeting properties.

134 abeled alpha-melanocyte-stimulating hormone (alpha-MSH) peptides could be used as imaging probes for

135 ugated alpha-melanocyte stimulating hormone (alpha-MSH) peptides.

136 ugated alpha-melanocyte stimulating hormone (alpha-MSH) peptides.

137 eptide alpha-melanocyte-stimulating hormone (alpha-MSH) promote satiety.

138 The alpha-melanocyte-stimulating hormone (alpha-MSH) receptor (melanocortin type 1 receptor [MC1R]

139 own as alpha-melanocyte-stimulating hormone (alpha-MSH) receptor, is an attractive molecular target f

140 ion of alpha-melanocyte-stimulating hormone (alpha-MSH) secretion by keratinocytes.

141 tes by alpha-melanocyte-stimulating hormone (alpha-MSH) stimulates cAMP signalling and melanin produc

142 ogs of alpha-melanocyte stimulating hormone (alpha-MSH) that function as melanocortin 1 receptor (MC1

143 grades alpha-melanocyte-stimulating hormone (alpha-MSH) to an inactive form that is unable to inhibit

144 block alpha-melanocyte-stimulating hormone (alpha-MSH) type 3 and 4 receptors, decreased LSNA in lep

145 ortin (alpha-melanocyte-stimulating hormone (alpha-MSH))-induced increase in the activities of adenyl

146 using alpha-melanocyte-stimulating hormone (alpha-MSH), an endogenous MC4R agonist, and agouti-relat

147 roduct alpha-melanocyte stimulating hormone (alpha-MSH), an MC3/4-R agonist, decreases food intake fo

148 CP-1), alpha-melanocyte stimulating hormone (alpha-MSH), and peroxisome proliferator-activated recept

149 gue of alpha-melanocyte stimulating hormone (alpha-MSH), exhibited high tumor concentration and rapid

150 log of alpha-melanocyte-stimulating hormone (alpha-MSH), has the potential for the detection of malig

151 s like alpha-melanocyte-stimulating hormone (alpha-MSH), neuropeptide Y (NPY), glutamate, and GABA fr

152 onist, alpha-melanocyte-stimulating hormone (alpha-MSH), or antagonist, SHU9119, in the third cerebra

153 MC4-R. alpha-Melanocyte stimulating hormone (alpha-MSH), the MC4-R agonist, administered intracerebro

154 igand, alpha-melanocyte stimulating hormone (alpha-MSH), to regulate TRH expression.

155 II) or alpha-melanocyte stimulating hormone (alpha-MSH), were unilaterally microinjected into the DMV

156 e that alpha-melanocyte-stimulating hormone (alpha-MSH), which is thought to be the mediator of UV re

157 lactam alpha-melanocyte-stimulating hormone (alpha-MSH)-derived Pro(6)-D-Phe(7)/D-Nal(2')(7)-Arg(8)-T

158 ion by alpha melanocyte-stimulating hormone (alpha-MSH)-synthesizing neurons of the arcuate nucleus,

159 onist, alpha-melanocyte stimulating hormone (alpha-MSH).

160 acetyl alpha-melanocyte-stimulating hormone (alpha-MSH).

161 active alpha-melanocyte-stimulating hormone (alpha-MSH).

162 igand, alpha-melanocyte stimulating hormone (alpha-MSH).

163 gonist alpha-melanocyte stimulating hormone (alpha-MSH).

164 igand, alpha-melanocyte-stimulating hormone (alpha-MSH).

165 els of alpha-melanocyte-stimulating hormone (alpha-MSH).

166 the agonist, melanocyte-stimulating hormone (alpha-MSH).

167 ulator alpha-melanocyte-stimulating hormone (alpha-MSH; referred to here as alpha-MSH1-13) undergoes

168 uch as alpha-melanocyte stimulation hormone (alpha-MSH).

169 CP has been shown to inactivate hypothalamic alpha-MSH, thus modulating melanocortin signaling in the

170 ation of mature PC1 and reduced hypothalamic alpha-MSH.

171 We sought to determine if alpha-MSH inhibits acute lung injury after renal ischemi

172 Although 75% of allografts in alpha-MSH-treated hosts survived at 70 days, 43% survive

173 trapeptide sequence, His-Phe-Arg-Trp, and in alpha-MSH it has been demonstrated further that a revers

174 f mononuclear and polymorphonuclear cells in alpha-MSH-treated mice compared with controls at days 7

175 showed a significantly reduced expression in alpha-MSH-treated mice compared with controls.

176 strogen, at least in part via an increase in alpha-MSH activity in the PVN.

177 ), Phe(261), His(264) in TM6 are involved in alpha-MSH binding and signaling.

178 ficant increase in corneal graft survival in alpha-MSH-treated recipients compared with controls.

179 Furthermore, SOM induced alpha-MSH production by the TCR-stimulated primed T cell

180 In normal animals, centrally injected alpha-MSH exerts a hyperthermic effect that is mediated

181 vation in nonpigmentary HaCaT keratinocytes (alpha-MSH, L-Lys-L-Pro-L-Val, and L-Lys-L-Pro-D-Val) and

182 nsive to its endogenous anorexigenic ligand, alpha-MSH.

183 ed using several melanocortin-based ligands [alpha-MSH, NDP-MSH, MTII, DNal (1')(7)-MTII, Nal(2')(7)-

184 An (18)F-labeled linear alpha-MSH peptide ((18)F-FB-Ac-Nle-Asp-His-d-Phe-Arg-Trp

185 hat the receptor-bound radioiodinated linear alpha-MSH analog NDP was released from the cells into th

186 , in vivo evidence that treatment with local alpha-MSH may significantly reduce allorejection of orth

187 decreased epidermal POMC processing and low alpha-MSH levels were documented previously.

188 Obese Zucker rats had lower alpha-MSH and dynorphin A(1-17) peptide levels in the pa

189 A number of alpha-melanotropin (alpha-MSH) analogues have been designed de novo, synthes

190 A number of novel alpha-melanotropin (alpha-MSH) analogues have been designed, synthesized, an

191 corticotropin (ACTH) and alpha-melanotropin (alpha-MSH)], and with somatolactin endocrine cells.

192 urons directly at the postsynaptic membrane, alpha-MSH and NPY potently stimulate and inhibit the cel

193 Moreover, alpha-MSH at physiologic doses significantly suppressed

194 ed and used to connect two high affinity NDP-alpha-MSH ligands or two low affinity MSH(4) ligands.

195 pared to the beta-turn-like structure at NDP-alpha-MSH (His(6)-d-Phe(7)-Arg(8)-Trp(9)).

196 We verified binding of Eu-DTPA-NDP-alpha-MSH to cells overexpressing the human melanocortin

197 )]-alpha-melanocyte-stimulating hormone (NDP-alpha-MSH) labeled with Eu(III)-DOTA was synthesized, an

198 7)]alpha-melanocyte-stimulating hormone (NDP-alpha-MSH) or forskolin-stimulated cAMP accumulation.

199 ermined by whole-cell binding of [(125)I]NDP-alpha-MSH, fluorescence immunocytochemistry and fluoresc

200 ed probe based on the superpotent ligand NDP-alpha-MSH, the monovalent and multivalent constructs app

201 Our results suggest that NDP-alpha-MSH and N-d-Nal(2')(7)-ACTH1-17 do not share the s

202 an affinity similar to that of unlabeled NDP-alpha-MSH and was used to optimize a competitive binding

203 d through competition with a nonradiolabeled alpha-MSH peptide analog, indicated the specific targeti

204 A number of novel alpha-MSH analogues were designed and synthesized primar

205 h quantitative reversal of hypothalamic NPY, alpha-MSH, and serotonin receptor (5-HT(1B)-receptor) en

206 alamic immunohistochemical study, using NPY, alpha-MSH, and 5-HT(1B)-receptor-specific antibodies and

207 ng synthetic analogue of naturally occurring alpha-MSH.

208 In the absence of alpha-MSH, a fraction of cell surface MC4R localized tog

209 ngs highlight a novel functional activity of alpha-MSH, which acts as a natural antiallergic basophil

210 olution, the neuroanatomical distribution of alpha-MSH in relation to AgRP was mapped in a teleost (z

211 t only prevented, but reversed the effect of alpha-MSH (1 microg) on Tc, thus resulting in augmented

212 s implies that the net antipyretic effect of alpha-MSH cannot be accounted for solely by modulation o

213 There was no effect of alpha-MSH on activated Caspase 9 and Caspase 3 while the

214 The effect of alpha-MSH on basophil activation was MC-1R mediated (as

215 as an anti-apoptotic factor, the effects of alpha-MSH on caspase activity, mitochondrial membrane po

216 Here we investigated the effects of alpha-MSH on the activity of supraoptic neurons.

217 the MC4R mediates the antipyretic effects of alpha-MSH.

218 In addition, expression of alpha-MSH was evaluated in ocular tissue by immunocytoch

219 m hypertensive levels to normal; infusion of alpha-MSH at the same rate had no effect.

220 g Kir7.1, independently of its inhibition of alpha-MSH binding.

221 th a pA(2) value of 7.9 in the inhibition of alpha-MSH-stimulated cAMP accumulation.

222 ctional activity and exhibited inhibition of alpha-MSH-stimulated cAMP production in cells expressing

223 ntracerebroventricular (i.c.v.) injection of alpha-MSH on lipopolysaccharide (LPS, 30 microg/kg i.p.)

224 raoptic neurons because central injection of alpha-MSH or selective MC4 receptor agonists inhibited t

225 dstream decreased after central injection of alpha-MSH.

226 Associated with the lack of alpha-MSH response in cultured uveal melanocytes was the

227 Much lower levels of alpha-MSH were secreted and only by the keratinocytes.

228 mia and to determine the early mechanisms of alpha-MSH action.

229 Moreover, oxidation of alpha-MSH can be prevented by the formation of a 1:1 com

230 oid receptors, and the core pharmacophore of alpha-MSH (His-Phe-Arg-Trp).

231 h of which lack the central pharmacophore of alpha-MSH.

232 esidues is very important for selectivity of alpha-MSH/gamma-MSH hybrids for hMCRs.

233 urthermore, amino acids at the N-terminal of alpha-MSH (Ser-Tyr-Ser) not considered to be part of the

234 esults demonstrate that adoptive transfer of alpha-MSH-generated IRBP-specific Treg cells promotes re

235 The carboxyl terminal tripeptides of alpha-MSH (KPV / KP-D-V) are the smallest minimal sequen

236 analogs were more potent than the former, or alpha-MSH, in stimulating the activity of tyrosinase, th

237 Bath application of MT-II or alpha-MSH significantly reduced spontaneous action poten

238 ed to renal ischemia treated with vehicle or alpha-MSH.

239 in the medial NTS by the endogenous peptide alpha-MSH, modulates gastric activity, which may have ph

240 peptide analogues: 125I-(Tyr2)-[Nle4, D-Phe7]alpha-MSH [125I-(Tyr2)-NDP]; 99mTc-CGCG-NDP; 99mTc-Gly11

241 ium (Tc)-labeled cyclic [Cys(3,4,10), D-Phe7]alpha-MSH(3-13) (CCMSH) exhibits high tumor uptake and r

242 ite of this increase, the level of pituitary alpha-MSH, a PCSK2 processing product, was unaltered.

243 t have been modified at the His(6) position (alpha-MSH numbering) and pharmacologically characterized

244 have been modified at the DPhe(7) position (alpha-MSH numbering) and pharmacologically characterized

245 t have been modified at the Trp(9) position (alpha-MSH numbering) and pharmacologically characterized

246 and levels of pituitary proopiomelanocortin/alpha-MSH, associated with decreased melanocortin-depend

247 secretion of appetite control hormones, PYY, alpha-MSH, and CART, are hampered.

248 itro and in vivo to develop radiohalogenated alpha-MSH peptide analogs with high tumor uptake, retent

249 in tumor-bearing mice with radiohalogenated alpha-MSH peptides showed very rapid tumor radioactivity

250 In afebrile rats, alpha-MSH infusion caused a modest transient increase in

251 UV-exposed keratinocytes secrete alpha-MSH, which then activates melanin formation in mel

252 ocular antigen) or ovalbumin (OVA)-specific alpha-MSH-induced Treg cells.

253 In this study, alpha-MSH, instead of being delivered extracellularly, i

254 d, with recipients receiving subconjunctival alpha-MSH or sham injections twice weekly.

255 zed and tested the effects of 3 tetrapeptide alpha-MSH analogs, Ac-His-D-Phe-Arg-Trp-NH2, n-Pentadeca

256 C5 receptors but is 30-fold more potent than alpha-MSH at the mMC4R.

257 cells, MC4R recycles constitutively and that alpha-MSH modulates MC4R residency at the plasma membran

258 We confirmed that alpha-MSH induces Fos expression in the supraoptic nucle

259 hen injected centrally and demonstrated that alpha-MSH also stimulates Fos expression in the nucleus

260 urons and we have recently demonstrated that alpha-MSH innervates TRH-synthesizing neurons in the hyp

261 s in the PVN, we raised the possibility that alpha-MSH may also participate in the mechanism by which

262 n-4 receptor (MC4R); existing data show that alpha-MSH is an agonist that couples the receptor to the

263 ary cells with the MC-1 receptor showed that alpha-MSH and the KPV peptides elevated intracellular ca

264 We have previously shown that alpha-MSH can inhibit tumor necrosis factor-alpha stimul

265 It has been shown by extensive studies that alpha-MSH bioactivity is critically dependent on the cor

266 These data suggest that alpha-MSH has an important role in the activation of pro

267 d in the supraoptic nucleus, suggesting that alpha-MSH and oxytocin actions are not independent.

268 ition of PGC-1alpha and PGC-1beta blocks the alpha-MSH-mediated induction of MITF and melanogenic gen

269 In addition, ICV coadministration of the alpha-MSH antagonist agouti-related peptide blocked the

270 ented ocular tissue lacked expression of the alpha-MSH ligand, as assessed by immunocytochemistry.

271 of this study was to conjugate CBTE2A to the alpha-MSH targeting ReCCMSH(Arg(11)) peptide for labelin

272 investigated in detail the ability of three alpha-MSH peptides to inhibit tumor necrosis factor alph

273 on in TUNEL staining by alpha-MSH is through alpha-MSH mediating suppression of the apoptotic pathway

274 Thus alpha-MSH-induced Fos expression is not associated with

275 thway to the PVN, but factors in addition to alpha-MSH also contribute to the mechanism by which lept

276 zes the conversion of adrenocorticotropin to alpha-MSH, thereby decreasing alpha-MSH peptide producti

277 Binding to alpha-MSH leads to stimulation of receptor activity and

278 d not change the MC4R dose-response curve to alpha-MSH, but it decreased the amount of cAMP generated

279 Ala-Phe-Dpr]-Tyr-NH(2) that is equipotent to alpha-MSH at the mMC1, mMC3, and mMC5 receptors but is 3

280 served in HaCaT keratinocytes in response to alpha-MSH (10(-15)-10(-7) M), KPV (10(-15)-10(-7) M), KP

281 lysis for growth and melanogenic response to alpha-MSH and expression of the receptor for alpha-MSH (

282 stimulation of proliferation in response to alpha-MSH at dosages ranging from 0.1 to 100 muM.

283 The rapidity and potency of the response to alpha-MSH in pigmentary and nonpigmentary cells suggest

284 or normal human keratinocytes in response to alpha-MSH, KPV or ACTH peptides.

285 required to maintain MC4R responsiveness to alpha-MSH by constantly eliminating from the plasma memb

286 t, whereas MRAP2b enhances responsiveness to alpha-MSH once the zebrafish begins feeding, thus increa

287 protein or HBD3 prohibited responsiveness to alpha-MSH, but not forskolin, suggesting receptor desens

288 ater than nine alkyl groups were superior to alpha-MSH in terms of the stimulation of human melanocyt

289 ds, but also yielded new biologically unique alpha-MSH analogues.

290 MT-II decreased phasic contractions, whereas alpha-MSH increased their amplitude.

291 SF, MT-II decreased neuronal firing, whereas alpha-MSH increased it.

292 es are required, which may be the reason why alpha-MSH was not able to bind hMC2R.

293 Treatment of basophils with alpha-MSH increased intracellular Ca(2+) but not cyclic

294 ta suggest that PVN NPY inputs converge with alpha-MSH to influence presympathetic neurons.

295 Treatment of human melanocytes with alpha-MSH results in stimulation of eumelanin synthesis,

296 ulated, arcuate nucleus-derived peptide with alpha-MSH antagonist activity, is contained in axon term

297 to determine the role of local therapy with alpha-MSH on corneal allograft survival, and the mechani

298 Treatment with alpha-MSH (1 microg, i.c.v.) suppressed LPS-induced incr

299 Brief treatment with alpha-MSH resulted in MC1R desensitization, whereas cont

300 natively activated macrophages where without alpha-MSH RPE induce apoptosis in the macrophages, which

301 Zebrafish alpha-MSH- and AgRP-immunoreactive (ir) cells are found