ライフサイエンスコーパス: MSH

1 MSH is produced by Mycobacterium tuberculosis, members o

2 MSH plays a key role in oxidative stress management and

3 for the wide range of lesions that activate MSH functions.

4 hereas ergothioneine does not; an additional MSH-dependent organic hydroperoxide peroxidase exists; a

5 ty NDP-alpha-MSH ligands or two low affinity MSH(4) ligands.

6 Alpha-MSH and ACTH are endogenous nonselective agonists for MC

7 alpha-MSH and other bioactive peptides are cleavage products o

8 alpha-MSH at physiologic doses potently suppressed basophil ac

9 alpha-MSH has anti-inflammatory properties in this in vitro gr

10 alpha-MSH increased the firing rate of MC3R VTA neurons in acu

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

12 alpha-MSH modulated the excitatory-inhibitory balance in the b

13 alpha-MSH preserves GAD67 expression and prevents loss of the

14 alpha-MSH signaling strongly induces PGC-1alpha expression and

15 alpha-MSH significantly increased the firing rate of VTA MC3R

16 alpha-MSH, melanotan II (MTII), and selective MC3R or MC4R ago

17 cid]-ReO-[Cys(3,4,10),d-Phe(7),Arg(11)]alpha-MSH(3-13) ((212)Pb-DOTA-Re(Arg(11))CCMSH) cured 45% of B

18 tide, ReO[Cys(3,4,10),d-Phe(7),Arg(11)]alpha-MSH(3-13) (ReCCMSH(Arg(11))), has shown high in vitro bi

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

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

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

22 ted that in-vitro-generated des-acetyl alpha-MSH successfully activated the melanocortin 4 receptor.

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

24 In addition, alpha-MSH did not improve mitochondrial membrane potential, ch

25 In addition, alpha-MSH promotes survival of the alternatively activated mac

26 In addition, alpha-MSH reduced gastric tone and mean arterial blood pressur

27 ltered anxiety that were rescued after alpha-MSH treatment.

28 antly, treatment with the MC1R agonist alpha-MSH or activation of the stress response kinase p38-MAPK

29 mina X are excited by the Mc4r agonist alpha-MSH, and acute inhibition of Mc4r signaling reduces loco

30 e that were responsive to the agonist, alpha-MSH, by 75%.

31 the hMC2R did not significantly alter alpha-MSH binding affinity and potency except substitution of

32 In this study, an alpha-MSH analog, Ac-Nle-Asp-His-D-Phe-Arg-Trp-Gly-Lys-NH(2) (

33 us regions of hMC2R were performed and alpha-MSH binding and signaling were examined.

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

35 of cathepsin L with beta-endorphin and alpha-MSH in the intermediate pituitary and with ACTH in the a

36 roduction of ACTH, beta-endorphin, and alpha-MSH peptide hormones in the regulated secretory pathway.

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

38 negative correlation between OX-A and alpha-MSH serum levels was found in obese mice as well as in h

39 decreases in ACTH, beta-endorphin, and alpha-MSH that were reduced to 23, 18, and 7% of wild-type con

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

41 roinjection of the agonists (MT-II and alpha-MSH) into the overlying nucleus of the solitary tract (N

42 cle melanocytes secreted both POMC and alpha-MSH, and this was enhanced in response to corticotrophin

43 adykinin, angiotensins II and III, and alpha-MSH, suggesting its role in the processing of tissue-spe

44 potential contribution of NPY/Y1R and alpha-MSH/MC3/4R-signaling to accumbens-induced high-fat feedi

45 Therefore, as alpha-MSH promotes the alternative activation of macrophages i

46 at intravenously injected biotinylated alpha-MSH phage were retained within melanoma tumors at 4 h af

47 hile AgRP binds competitively to block alpha-MSH binding and blocks the constitutive activity mediate

48 Although ASIP and HBD3 each blocked alpha-MSH-mediated induction of the signaling pathway, only AS

49 perphagia, and weight gain by blunting alpha-MSH production via CB1R-induced and extracellular-signal

50 eta-amyloid peptide load in the brain, alpha-MSH improves spatial memory in TgCRND8 mice and prevents

51 r nucleus of the hypothalamus (PVN) by alpha-MSH and AgRP can be mediated independently of Galphas si

52 intra-VTA alpha-MSH may be mediated by alpha-MSH changing the activity of MC3R-expressing VTA neurons

53 at the diminution in TUNEL staining by alpha-MSH is through alpha-MSH mediating suppression of the ap

54 satiety circuit, and its modulation by alpha-MSH, provides insight into regulation of hunger and sati

55 spinal lamina X that are inhibited by alpha-MSH, which is in line with previous studies in rodents w

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

57 el radiolabeled lactam bridge-cyclized alpha-MSH peptide for melanoma imaging and treatment.

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

59 ropin to alpha-MSH, thereby decreasing alpha-MSH peptide production.

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

61 c littermates were treated with either alpha-MSH or vehicle via daily intraperitoneal injections for

62 y inhibited by coinjection with excess alpha-MSH peptide (P < 0.05), indicating that (18)F-FB-NAPamid

63 d TM6 of the hMC4R are responsible for alpha-MSH binding and signaling.

64 es in TMs of the hMC4R are crucial for alpha-MSH binding and signaling.

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

66 ide is a promising molecular probe for alpha-MSH receptor-positive melanoma PET and warrants further

67 Furthermore, alpha-MSH and AgRP-ir somata and fibers are pronounced at 5 da

68 alpha-melanocyte-stimulating hormone (alpha-MSH) analogues which are N-terminal modified with a long

69 alpha-melanocyte-stimulating hormone (alpha-MSH) and its endogenous antagonist, agouti-related prote

70 alpha-melanocyte stimulating hormone (alpha-MSH) and orexigenic Agouti-related protein (AgRP) from d

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

72 alpha-melanocyte stimulating hormone (alpha-MSH) are synthesized by proteolytic processing of their

73 alpha-melanocyte stimulating hormone (alpha-MSH) attenuates GABAergic loss and thus improves cogniti

74 lpha-melanocortin-stimulating hormone (alpha-MSH) binding, in this study, we utilized both receptor d

75 alpha-melanocyte-stimulating hormone (alpha-MSH) from ex vivo hypothalamic explants.

76 alpha-melanocyte-stimulating hormone (alpha-MSH) inhibit and stimulate, respectively, PVN-RVLM neuro

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

78 alpha-Melanocyte stimulating hormone (alpha-MSH) is a neuropeptide that suppresses host inflammatory

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

80 alpha-melanocyte stimulating hormone (alpha-MSH) is an important regulator of immune cell activity w

81 alpha-melanocyte-stimulating hormone (alpha-MSH) is reduced, yet the mRNA of its precursor protein p

82 alpha-melanocyte-stimulating hormone (alpha-MSH) of pars intermedia melanotropes, provides a unique

83 alpha-melanocyte-stimulating hormone (alpha-MSH) on basophil function.

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

85 t that melanocyte-stimulating hormone (alpha-MSH) or ACTH induce ATR-pS435, enhance XPA's association

86 alpha-melanocyte-stimulating hormone (alpha-MSH) peptide analogs.

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

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

89 alpha-melanocyte stimulating hormone (alpha-MSH) peptides.

90 alpha-melanocyte stimulating hormone (alpha-MSH) peptides.

91 alpha-melanocyte-stimulating hormone (alpha-MSH) promote satiety.

92 alpha-melanocyte-stimulating hormone (alpha-MSH) receptor (melanocortin type 1 receptor [MC1R]) is o

93 alpha-melanocyte-stimulating hormone (alpha-MSH) receptor, is an attractive molecular target for mel

94 alpha-melanocyte-stimulating hormone (alpha-MSH) secretion by keratinocytes.

95 alpha-melanocyte-stimulating hormone (alpha-MSH) stimulates cAMP signalling and melanin production a

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

97 alpha-melanocyte-stimulating hormone (alpha-MSH) type 3 and 4 receptors, decreased LSNA in leptin-tr

98 (alpha-melanocyte-stimulating hormone (alpha-MSH))-induced increase in the activities of adenylate cy

99 alpha-melanocyte stimulating hormone (alpha-MSH), and peroxisome proliferator-activated receptor-gam

100 alpha-melanocyte-stimulating hormone (alpha-MSH), has the potential for the detection of malignant m

101 alpha-melanocyte-stimulating hormone (alpha-MSH), neuropeptide Y (NPY), glutamate, and GABA from fir

102 alpha-melanocyte stimulating hormone (alpha-MSH), were unilaterally microinjected into the DMV of ra

103 alpha-melanocyte-stimulating hormone (alpha-MSH)-derived Pro(6)-D-Phe(7)/D-Nal(2')(7)-Arg(8)-Trp(9)-

104 alpha-melanocyte-stimulating hormone (alpha-MSH).

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

106 alpha-melanocyte-stimulating hormone (alpha-MSH).

107 alpha-melanocyte stimulating hormone (alpha-MSH).

108 alpha-melanocyte-stimulating hormone (alpha-MSH).

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

110 dvancement in the understanding of how alpha-MSH acts in the VTA to affect feeding and food reward.

111 sults help us to better understand how alpha-MSH acts in the VTA to affect feeding and other dopamine

112 To determine how alpha-MSH acts in the VTA to affect feeding, we performed elec

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

114 been shown to inactivate hypothalamic alpha-MSH, thus modulating melanocortin signaling in the contr

115 n, at least in part via an increase in alpha-MSH activity in the PVN.

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

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

118 nuclear and polymorphonuclear cells in alpha-MSH-treated mice compared with controls at days 7 and 14

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

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

121 to its endogenous anorexigenic ligand, alpha-MSH.

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

123 ivo evidence that treatment with local alpha-MSH may significantly reduce allorejection of orthotopic

124 otropin (ACTH) and alpha-melanotropin (alpha-MSH)], and with somatolactin endocrine cells.

125 directly at the postsynaptic membrane, alpha-MSH and NPY potently stimulate and inhibit the cells, re

126 Moreover, alpha-MSH at physiologic doses significantly suppressed secret

127 nulomas were treated daily with 10 muM alpha-MSH or saline as control.

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

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

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

131 ha-melanocyte-stimulating hormone (NDP-alpha-MSH) labeled with Eu(III)-DOTA was synthesized, and the

132 be based on the superpotent ligand NDP-alpha-MSH, the monovalent and multivalent constructs appear to

133 ugh competition with a nonradiolabeled alpha-MSH peptide analog, indicated the specific targeting of

134 thetic analogue of naturally occurring alpha-MSH.

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

136 .1, independently of its inhibition of alpha-MSH binding.

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

138 n, the neuroanatomical distribution of alpha-MSH in relation to AgRP was mapped in a teleost (zebrafi

139 There was no effect of alpha-MSH on activated Caspase 9 and Caspase 3 while there was

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

141 anti-apoptotic factor, the effects of alpha-MSH on caspase activity, mitochondrial membrane potentia

142 Finally, we show that the effect of alpha-MSH on MC3R neuron firing rate is probably activity-depe

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

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

145 ghlight a novel functional activity of alpha-MSH, which acts as a natural antiallergic basophil-respo

146 demonstrate that adoptive transfer of alpha-MSH-generated IRBP-specific Treg cells promotes retinal

147 hich lack the central pharmacophore of alpha-MSH.

148 Bath application of MT-II or alpha-MSH significantly reduced spontaneous action potentials

149 e medial NTS by the endogenous peptide alpha-MSH, modulates gastric activity, which may have physiolo

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

151 ion of appetite control hormones, PYY, alpha-MSH, and CART, are hampered.

152 UV-exposed keratinocytes secrete alpha-MSH, which then activates melanin formation in melanocyt

153 r antigen) or ovalbumin (OVA)-specific alpha-MSH-induced Treg cells.

154 In this study, alpha-MSH, instead of being delivered extracellularly, is targ

155 h recipients receiving subconjunctival alpha-MSH or sham injections twice weekly.

156 ceptor (MC4R); existing data show that alpha-MSH is an agonist that couples the receptor to the Galph

157 Injection of the alpha-MSH analog MTII into the ventral tegmental area (VTA) de

158 addition, ICV coadministration of the alpha-MSH antagonist agouti-related peptide blocked the anorex

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

160 s study was to conjugate CBTE2A to the alpha-MSH targeting ReCCMSH(Arg(11)) peptide for labeling to (

161 In addition, the alpha-MSH-induced increase in MC3R neuron activity was indepen

162 of PGC-1alpha and PGC-1beta blocks the alpha-MSH-mediated induction of MITF and melanogenic genes.

163 TUNEL staining by alpha-MSH is through alpha-MSH mediating suppression of the apoptotic pathway that

164 red to maintain MC4R responsiveness to alpha-MSH by constantly eliminating from the plasma membrane a

165 developed granulomas after exposure to alpha-MSH compared with saline treated granulomas.

166 Binding to alpha-MSH leads to stimulation of receptor activity and suppre

167 reas MRAP2b enhances responsiveness to alpha-MSH once the zebrafish begins feeding, thus increasing t

168 change the MC4R dose-response curve to alpha-MSH, but it decreased the amount of cAMP generated per r

169 n or HBD3 prohibited responsiveness to alpha-MSH, but not forskolin, suggesting receptor desensitizat

170 e conversion of adrenocorticotropin to alpha-MSH, thereby decreasing alpha-MSH peptide production.

171 ggesting that the effects of intra-VTA alpha-MSH may be mediated by alpha-MSH changing the activity o

172 -II decreased neuronal firing, whereas alpha-MSH increased it.

173 decreased phasic contractions, whereas alpha-MSH increased their amplitude.

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

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

176 termine the role of local therapy with alpha-MSH on corneal allograft survival, and the mechanisms by

177 Treatment with alpha-MSH promoted a significantly higher concentration of p-C

178 Brief treatment with alpha-MSH resulted in MC1R desensitization, whereas continuous

179 gest that PVN NPY inputs converge with alpha-MSH to influence presympathetic neurons.

180 ly activated macrophages where without alpha-MSH RPE induce apoptosis in the macrophages, which is se

181 Zebrafish alpha-MSH- and AgRP-immunoreactive (ir) cells are found in dis

182 iscovered that the disruption of TgMSH-1, an MSH in the pathogenic parasite, Toxoplasma gondii, confe

183 ns, enzymes involved in MSH biosynthesis and MSH-dependent detoxification are targets for drug develo

184 ortality in SCA: two adult trials (LaSHS and MSH) and one pediatric study (Brazilian cohort).

185 ins, demonstrating its ability to antagonize MSH agonists at central MC3/4-R, but did not produce an

186 then evaluated if seasonal patterns found at MSH matched those reported at Columbia University Medica

187 lower potency than ACTH, alpha-MSH, and beta-MSH.

188 ensin 3 and agouti signaling protein blocked MSH- but not forskolin-mediated enhancement of platinum-

189 ast) then survey the genome for lesion-bound MSH proteins.

190 Protein S-mycothiolation was accompanied by MSH depletion in the thiol-metabolome.

191 they too bind ATP and are targeted to MMR by MSH sliding clamps.

192 MSH-free preconditioned medium, the cellular MSH was catabolized to generate GlcN-Ins and AcCys.

193 Accordingly, mammalian cells lacking certain MSHs are resistant to chemotherapeutic drugs.

194 the corresponding parental ligand, CH(3)(CO)-MSH(4)-NH(2).

195 tiple copies of the azide N(3)(CH(2))(5)(CO)-MSH(4)-NH(2) were attached to the alkyne-bearing, solane

196 and, CH(3)(CH(2))(3)(C(2)N(3))(CH(2))(5)(CO)-MSH(4)-NH(2), was not significantly diminished relative

197 R(CO)-MSH(4)-NH(2) ligands, which have a relatively low affini

198 mutants were incubated in medium containing MSH, they actively transported it to generate cellular l

199 also shown that, unlike previously described MSHs involved in signalling, TgMSH-1 localizes to the pa

200 gamma-MSH (gamma-melanocyte-stimulating hormone, H-Tyr-Val-Met

201 ed a peptide, [Leu(3), Leu(7), Phe(8)]-gamma-MSH-NH2 (compound 5), which is 16-fold selective for the

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

203 have engineered peptides by cyclizing gamma-MSH using a thioether bridge.

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

205 acophores of MTII, SHU9119, and Ac-NDP-gamma-MSH-NH(2) replaced by Pro or trans-/cis-4-guanidinyl-Pro

206 istration of an MC(3) agonist, D[Trp8]-gamma-MSH, attenuated disease incidence and severity in wild-t

207 A number of novel cyclic truncated gamma-MSH analogues were designed and synthesized, in which a

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

209 einyl)amido-2-deoxy-alpha-d-glucopyranoside (MSH or AcCys-GlcN-Ins), to act against oxidative and ant

210 einyl)amido-2-deoxy-alpha-D-glucopyranoside (MSH or AcCys-GlcN-Ins).

211 c acid were marginally significantly higher (MSH) in PF-H samples.

212 ules, which can be detected by MutS homolog (MSH) mismatch repair protein heterodimers.

213 Highly conserved MutS homologs (MSH) and MutL homologs (MLH/PMS) are the fundamental com

214 matches and lesions activate MutS homologue (MSH) ATPase activity that is essential for mismatch repa

215 MutS homologues (MSHs) are critical components of the eukaryotic mismatch

216 nerated alpha-melanocyte stimulated hormone (MSH)-induced Treg cells specific to ocular autoantigen s

217 MC1R ligand melanocyte stimulating hormone (MSH) or by pharmacologic cAMP induction by forskolin enh

218 Melanocyte-stimulating hormone (MSH) peptides processed from proopiomelanocortin (POMC)

219 Melanocyte-stimulating hormone (MSH) plays a crucial role in pigment cell differentiatio

220 Melanocyte-stimulating hormone (MSH) reduces UV-induced DNA damage through the induction

221 s induced by melanocyte-stimulating hormone (MSH).

222 Trp(8)-gamma-melanocyte stimulating hormone (MSH; DTrp).

223 nd gamma(2)-melanocyte stimulating hormones (MSH) and adrenocorticotropin (ACTH)], the antagonist ago

224 and gamma2-melanocyte stimulating hormones (MSH) and adrenocorticotropin hormone (ACTH).

225 ,169,599 patients from Mount Sinai Hospital (MSH) to compute phenome-wide associations between birth

226 that sequence contexts that provoke improved MSH-activation displayed enhanced localized DNA flexibil

227 substitution of Phe(7) with d-Nal(2')(7) in MSH in hMC1R, hMC3R, and hMC4R.

228 deoxy-alpha-D-glucopyranoside and acetate in MSH biosynthesis.

229 f hormones is mediated by cAMP: High cAMP in MSH-treated cells stimulates PKA, whereas low cAMP in me

230 ese important functions, enzymes involved in MSH biosynthesis and MSH-dependent detoxification are ta

231 Consequently, the enzymes involved in MSH biosynthesis are targets for drug development.

232 side and acetate, the fourth overall step in MSH biosynthesis.

233 increases in binding potency with increased MSH(4) content per scaffold were observed.

234 In keratinocytes, MSH bound to the melanocyte melanocortin receptor type 1

235 An mshA(G32D) mutant lacking MSH overproduced ergothioneine but not Ohr.

236 synthetic htMVLs that contain melanocortin (MSH) and cholecystokinin (CCK) pharmacophores that are c

237 nduced by O-mesitylenesulfonylhydroxylamine (MSH) and is compatible with methionine.

238 provide the first example of a mitochondrial MSH that is involved in drug sensitivity and implicate t

239 Highly conserved MutS (MSH) and MutL (MLH/PMS) homologues initiate mismatch rep

240 match and damage recognition domains of MutS/MSH and NER helicase XPB, respectively, as well as with

241 Mycothiol (MSH) is the major low molecular weight (LMW) thiol in Ac

242 Mycothiol (MSH) is the major thiol in Actinobacteria and plays a ro

243 Mycothiol (MSH) is the principal low-molecular-weight thiol, unique

244 nstead utilize the small molecule mycothiol (MSH) as their primary reducing agent and for the detoxif

245 a that utilize the small molecule mycothiol (MSH) as their primary reducing agent.

246 f the actinomycete family produce mycothiol (MSH or acetylcysteine-glucosamine-inositol, AcCys-GlcN-I

247 terium smegmatis does not produce mycothiol (MSH) and was found to markedly overproduce both ergothio

248 the major M. tuberculosis thiol, mycothiol (MSH), are required to resist acidic stress during infect

249 Mycothiol ([MSH] AcCys-GlcN-Ins, where Ac is acetyl) is the major th

250 n hAGRP(87-132), and synthetic agonists [NDP-MSH, MTII, and the tetrapeptide Ac-His-dPhe-Arg-Trp-NH(2

251 e7]alpha-melanocyte stimulating hormone (NDP-MSH) ligands is reported.

252 )]-alpha-melanocyte stimulating hormone (NDP-MSH), a potent non-steroidogenic pan-melanocortin recept

253 e7]alpha-melanocyte-stimulating hormone (NDP-MSH), by first defining the role of the His6-d-Phe7-Arg8

254 D-Phe(7)]melanocyte-stimulating hormone (NDP-MSH), thereby differentiating between residues directly

255 e ligands examined in this study include NDP-MSH, MTII, Ac-His-DPhe-Arg-Trp-NH2 (JRH887-9), Ac-Anc-DP

256 anding of the binding mode of the ligand NDP-MSH at the atomic level.

257 Based on a model of NDP-MSH and MC4R interaction, the antagonist behavior of the

258 ractions between the terminal regions of NDP-MSH and the receptor are described.

259 ted mutagenesis and a molecular model of NDP-MSH bound to the active state of the receptor.

260 over, in complementary in vitro studies, NDP-MSH attenuated the lipopolysaccharide elicited apoptosis

261 These studies resulted in the NDP-MSH, MTII, AMW3-130, THIQ, and AMW3-106 ligands possessi

262 vo using mouse models that lack all neuronal MSH, thereby precluding competitive antagonism of MC-R b

263 n mutant Tn1) of MSH biosynthesis produce no MSH.

264 The absence of MSH resulted in a higher basal oxidation level of 338 Cy

265 associated with both Ohr and the absence of MSH.

266 The biosynthesis of MSH is essential for cell growth and has been proposed t

267 The biosynthesis of MSH is essential for cell growth, and therefore, the MSH

268 The biosynthesis of MSH proceeds via a five-step process that involves four

269 did not accurately predict the hierarchy of MSH ATPase activation.

270 nergy balance via a mechanism independent of MSH and MC3/4-R competitive antagonism, consistent with

271 Intracutaneous injection of MSH prevented UV-induced DNA damage in human and mouse s

272 ransported it to generate cellular levels of MSH comparable to or greater than the normal content of

273 The half-life of MSH was determined in stationary phase cells to be appro

274 However, the collaborative mechanics of MSH and MLH/PMS proteins have not been resolved in any o

275 train 49) or MshC (transposon mutant Tn1) of MSH biosynthesis produce no MSH.

276 milar assay with a Eu-labeled probe based on MSH(4), modest increases in binding potency with increas

277 ow-abundance tissue markers such as Bcl-6 or MSH-6.

278 ence demonstrating that UV induction of POMC/MSH in skin is directly controlled by p53.

279 The activation of p53-POMC/MSH-MC1R signaling is required for the UV-induced melano

280 ignaling pathway interacts with the p53-POMC/MSH-MC1R signaling pathway, and both are crucial in mela

281 cysteine desulfhydrase or used to regenerate MSH in cells with active MshC.

282 The resulting MSH-MLH complex formed at a DNA lesion initiates downstr

283 xpressed only one (control) or both (target) MSH and CCK receptors.

284 In this study, we provide evidence that MSH also enhances DNA repair in skin keratinocytes by mo

285 ce for growth of M. smegmatis, indicate that MSH functions not only as a protective cofactor but also

286 match repair (MMR) models have proposed that MSH (MutS homolog) proteins identify DNA polymerase erro

287 Our results further reveal that MSH is important to maintain the reduced state of protei

288 n the MshC-deficient mutant, suggesting that MSH biosynthesis may be a suitable target for drugs to t

289 The MSH biosynthetic enzymes present potential targets for i

290 Furthermore, inactivation of the MSH pathway subverted the expression of whiB3 along with

291 sphodiesterase 4D3 as a direct target of the MSH/cAMP/MITF pathway.

292 decades of debate, it appears clear that the MSH proteins initiate MMR by recognizing a mismatch and

293 ssential for cell growth, and therefore, the MSH biosynthetic enzymes present potential targets for i

294 When these MSH-loaded mutants were transferred to MSH-free precondi

295 educing environment by reducing MSSM back to MSH.

296 these MSH-loaded mutants were transferred to MSH-free preconditioned medium, the cellular MSH was cat

297 ntation-independent mechanism that underlies MSH-mediated DNA repair following UVB irradiation.

298 Using MSH labeled with [U-(14)C]cysteine or with [6-(3)H]GlcN,

299 ere SH in BWF-H sunflower honey; butanal was MSH, and 2-phenylethanol was more abundant in BWF-H blac

300 Treatment of the resulting thioether with MSH results in regeneration of dehydroalanine, allowing