ライフサイエンスコーパス: alpha-MSH

1 alpha-MSH and other bioactive peptides are cleavage prod

2 alpha-MSH at physiologic doses potently suppressed basop

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

4 alpha-MSH has anti-inflammatory properties in this in vi

5 alpha-MSH increased the firing rate of MC3R VTA neurons

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 significantly increased the firing rate of VTA

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

37 in lamina X are excited by the Mc4r agonist alpha-MSH, and acute inhibition of Mc4r signaling reduce

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

59 0 nM), the analogue obtained is as potent as alpha-MSH in the frog skin MC1R assay.

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

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

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

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

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

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

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

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

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

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

70 ons in spinal lamina X that are inhibited by alpha-MSH, which is in line with previous studies in rod

71 ts of intra-VTA alpha-MSH may be mediated by alpha-MSH changing the activity of MC3R-expressing VTA n

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

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

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

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

76 are innervated by axon terminals containing alpha-MSH.

77 were contacted by axon terminals containing alpha-MSH.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

118 alpha-melanocyte stimulating hormone (alpha-MSH) is a melanocortin signaling peptide with anti

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

120 Alpha-melanocyte stimulating hormone (alpha-MSH) is an anorexigenic peptide.

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

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

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

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

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

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

127 ra-VTA alpha-melanocyte stimulating hormone (alpha-MSH) on feeding and food reward are unknown.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

163 To determine how alpha-MSH acts in the VTA to affect feeding, we performe

164 tant advancement in the understanding of how alpha-MSH acts in the VTA to affect feeding and food rew

165 orescent protein in MC3R neurons to test how alpha-MSH affects the activity of VTA MC3R neurons.

166 ese results help us to better understand how alpha-MSH acts in the VTA to affect feeding and other do

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

190 Moreover, alpha-MSH at physiologic doses significantly suppressed

191 ed granulomas were treated daily with 10 muM alpha-MSH or saline as control.

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

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

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

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

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

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

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

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

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

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

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

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

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

205 ng synthetic analogue of naturally occurring alpha-MSH.

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

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

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

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

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

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

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

213 Finally, we show that the effect of alpha-MSH on MC3R neuron firing rate is probably activit

214 We aimed to evaluate the effects of alpha-MSH in a novel in vitro sarcoidosis model.

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 anti-inflammatory effects of alpha-MSH were blocked by specific p-CREB inhibition.

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

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

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

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

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

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

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

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

226 dstream decreased after central injection of alpha-MSH.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

264 The alpha-MSH induced increase in MC3R neuron firing rate is

265 In addition, the alpha-MSH-induced increase in MC3R neuron activity was i

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

267 Injection of the alpha-MSH analog MTII into the ventral tegmental area (V

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

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

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

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

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

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

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

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

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

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

278 ed in developed granulomas after exposure to alpha-MSH compared with saline treated granulomas.

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

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

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

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

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

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

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

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

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

288 TA, suggesting that the effects of intra-VTA alpha-MSH may be mediated by alpha-MSH changing the acti

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

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

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

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

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

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

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

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

297 Treatment with alpha-MSH promoted a significantly higher concentration

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

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

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