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 is a potent agonist at hMC4R but not at hMC2R.

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

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

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

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

14 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

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

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

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

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

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

20 -mediated oxidation of epidermal ACTH, alpha-MSH, and beta-endorphin in vitiligo owing to oxidation o

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

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

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

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

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

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

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

28 ionality using the endogenous agonists alpha-MSH, beta-MSH, gamma2-MSH, ACTH(1-24), the antagonist hA

29 ent than the other endogenous agonists alpha-MSH, gamma2-MSH, ACTH(1-24).

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

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

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

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

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

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

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

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

38 d the expression of MC1R under UVR and alpha-MSH stimulation in skin of different ethnic origins and

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

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

54 RP-1, and TRP-2 were not influenced by alpha-MSH.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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 neuropeptide that suppresses host inflammatory

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

114 to its endogenous anorexigenic ligand, alpha-MSH.

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

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

117 ased epidermal POMC processing and low alpha-MSH levels were documented previously.

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

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

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

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

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

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

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

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

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

127 thetic analogue of naturally occurring alpha-MSH.

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

129 .1, independently of its inhibition of alpha-MSH binding.

130 Moreover, oxidation of alpha-MSH can be prevented by the formation of a 1:1 complex w

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

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

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

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

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

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

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

138 hich lack the central pharmacophore of alpha-MSH.

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

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

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

142 evels of pituitary proopiomelanocortin/alpha-MSH, associated with decreased melanocortin-dependent be

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

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

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

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

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

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

149 MC4R recycles constitutively and that alpha-MSH modulates MC4R residency at the plasma membrane by a

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

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

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

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

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

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

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

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

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

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

160 t also yielded new biologically unique alpha-MSH analogues.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

176 y, at the N97D, L106P, and C271Y hMC4Rs beta-MSH was more potent than the other endogenous agonists a

177 sing the endogenous agonists alpha-MSH, beta-MSH, gamma2-MSH, ACTH(1-24), the antagonist hAGRP(87-132

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

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

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

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

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

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

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

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

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

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

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

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

190 -Cys-GlcN-Ins serves as a weak surrogate for MSH but is not sufficient to support normal growth of M.

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

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

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

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

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

196 nti-inflammatory effects of [d-Trp(8)]-gamma-MSH.

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

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

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

200 administration of 3-30 microg [D-Trp8]-gamma-MSH significantly inhibited leukocyte influx and cytokin

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

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

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

204 ogenous agonists alpha-MSH, beta-MSH, gamma2-MSH, ACTH(1-24), the antagonist hAGRP(87-132), and the s

205 other endogenous agonists alpha-MSH, gamma2-MSH, ACTH(1-24).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

220 ,169,599 patients from Mount Sinai Hospital (MSH) to compute phenome-wide associations between birth

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

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

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

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

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

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

227 while disruption in the mshB gene results in MSH levels 20 to 100% of those of the wild type.

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

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

230 mphasize the essential role of intercellular MSH signalling in the tanning response, and suggest a cl

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

247 AGRP(87-132), and the synthetic agonists NDP-MSH and MTII.

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

249 ith alanine also significantly decreased NDP-MSH binding and receptor activity, (iii) substitutions o

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

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

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

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

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

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

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

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

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

259 in TM6 with alanine dramatically reduced NDP-MSH binding affinity and receptor signaling, (ii) substi

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 aviolet light potently induces expression of MSH in keratinocytes, but fails to stimulate pigmentatio

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

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

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

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

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

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

276 The production of MSH provides a potential novel target for tuberculosis t

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

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

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

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

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

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

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

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

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

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

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

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

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

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

291 The MSH biosynthetic enzymes present potential targets for i

292 mmon in patients in the NIH study and in the MSH cohort.

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

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

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

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

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

298 educing environment by reducing MSSM back to MSH.

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

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

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

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