ライフサイエンスコーパス: GHS

1 GHS is caused by altered expression of genes encoding ne

2 GHS x WKY rats were backcrossed to breed for congenic ra

3 GHS-R1a antagonism has therefore been proposed as a pote

4 GHS-R1a signals through Gq, Gi/o, G13, and arrestin.

5 GHS-R1a-G-protein coupling and the formation of GHS-R1a:

6 GHS-R1a:GHS-R1b:D5R oligomers were first demonstrated in

7 From baseline to week 12, GHS/QOL scores were maintained with both pembrolizumab p

8 Two human GPC-Rs related to both the type 1a GHS-R and NT-Rs were cloned and characterized.

9 the growth hormone secretagogue receptor 1a (GHS-R1a) and the cluster of differentiation 36 (CD36) re

10 the growth hormone secretagogue receptor 1a (GHS-R1a), is a G-protein-coupled receptor that is differ

11 eceptor growth hormone secretagogue type 1a (GHS-R1a) in the hypothalamus and pituitary.

12 rowth hormone secretagogue receptor type 1a (GHS-R1a), in VP neurons caused the dendritic release of

13 rowth hormone secretagogue receptor type 1a (GHS-R1a), is considered to be the active form for its or

14 rowth hormone secretagogue receptor type 1a (GHS-R1a), is mainly secreted from the stomach and regula

15 rmed residuals in urinary calcium in an F(2) GHS x WKY mapping cohort.

16 From baseline to week 21, GHS/QOL scores were better maintained with pembrolizumab

17 The Ni-N(4) /GHSs/Fe-N(4) endows a rechargeable Zn-air battery with e

18 The developed Ni-N(4) /GHSs/Fe-N(4) Janus material exhibits excellent bifunctio

19 hich suggests another possible benefit for a GHS-R1a antagonist, namely, the role as an insulin secre

20 e was confirmed by treating MENX rats with a GHS-R1a antagonist.

21 However, ghrelin also activates GHS-R1A receptors on extrahypothalamic targets that medi

22 de that stimulates food intake by activating GHS-R1A receptors in the hypothalamus.

23 All GHS rats received a fixed amount of a standard 1.2% calc

24 d 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] and GHS rats have increased renal vitamin D receptor content

25 f DHFR docked with our GHS-R antagonists and GHS-R modeling, we designed and synthesized a series of

26 supporting the potential use of ghrelin and GHS-R agonists in the management of disease-associated c

27 The relevance of ghrelin and GHS-R expression was verified in clinically relevant tis

28 3 weeks (n=11); (2) chronic rapid pacing and GHS (CP-424,391 at 10 mg x kg(-1) x d(-1), n=9); and (3)

29 ly meaningful improvements in worst pain and GHS/QOL with enfortumab vedotin plus pembrolizumab.

30 Differential co-expression of GHS-R1a and GHS-R1b, both in HEK-293T cells and in striatal and hipp

31 ity constants for GHR/GHS-R1a and antagonist/GHS-R1a in the absence of G proteins are in good agreeme

32 f 16,169 European individuals from the ARIC, GHS, MARTHA and PROCARDIS studies, were meta-analysed an

33 This demonstrates that bias at GHS-R1a signaling can occur not only with regard to agon

34 ast 1 note (84% at BIDMC, 82% [corrected] at GHS, and 47% at HMC).

35 To delineate ligand selectivity at GHS-R1a signaling, we analyzed in detail the efficacy of

36 the non-CNS penetrant inverse agonist 22 (AZ-GHS-22) and the CNS penetrant inverse agonist 38 (AZ-GHS

37 and the CNS penetrant inverse agonist 38 (AZ-GHS-38).

38 Previously, 2,4-diaminopyrimidine-based GHS-R antagonists reported from our laboratories have be

39 n x time, B [95% CI]), adjusted for baseline GHS/QOL scores, and age, sex, stage, and treatment modal

40 an Galpha(q11) requires interactions between GHS-R1a and SST receptor subtype 5 (SST5) and that in th

41 Biasing GHS-R1a signaling with specific ligands may lead to the

42 shortest ghrelin analogue capable of binding GHS-R1a with better affinity than ghrelin(1-28).

43 3 administration increased renal CaR in both GHS and NC rats.

44 a greater reduction in HRQOL, as measured by GHS, compared with radiotherapy at 24 months.

45 s effect on insulin secretion is mediated by GHS-R in pancreatic beta-cells.

46 e for the primary PRO variable EORTC QLQ-C30 GHS (14.1 months [95% CI 10.4-18.7] vs 5.9 months [4.3-7

47 prespecified primary domains: EORTC QLQ-C30 GHS-quality of life (QoL), physical functioning, cogniti

48 -0.02; nominal p=0.041) and in EORTC QLQ-C30 GHS/QOL (least squares mean change: enfortumab vedotin p

49 s mean baseline-to-week-15 change in QLQ-C30 GHS/QOL score was 6.9 (95% CI 3.3 to 10.6) for pembroliz

50 ally meaningful improvement in EORTC QLQ-C30 GHS/QOL scores with pembrolizumab versus chemotherapy (b

51 edian time to deterioration in EORTC QLQ-C30 GHS/QOL was 24.9 months (95% CI 13.8 to not reached) in

52 -0.77], log-rank p<0.0001) for EORTC QLQ-C30 GHS/QOL, and 124.86 weeks (94.71-134.57) versus 74.86 we

53 74-1.05], log-rank p=0.17) for EORTC QLQ-C30 GHS/QOL, and 9.43 weeks (6.43-12.29) versus 9.14 weeks (

54 gomerization of GHS-R1a with D1R, conferring GHS-R1a distinctive pharmacological properties.

55 wth hormone secretagogue receptor-deficient (GHS-R-deficient) mice displayed enhanced age-associated

56 tion of the GHS-R by structurally dissimilar GHSs, was conserved in GPR38 and GPR39.

57 pound 2 is a potent, novel, orally effective GHS that shows an excellent safety profile in preclinica

58 In DESTINY-Breast03, EORTC GHS/QoL was maintained on both therapies throughout trea

59 on inhibits GHS-R1a function by facilitating GHS-R1a trafficking to the plasma membrane and by exerti

60 fication of a genomic clone encoding a first GHS-R/NT-R family member (GPR38).

61 2.31 to 16.56) and 6.49 (-0.43 to 13.41) for GHS-QoL, and 5.38 (-0.01 to 10.78) and 6.34 (1.07 to 11.

62 r with pembrolizumab versus chemotherapy for GHS/QOL (hazard ratio 0.61 [95% CI 0.38-0.98]; one-sided

63 ix to 8 weeks later, rats were evaluated for GHS and tissue was collected for molecular experiments.

64 deficits was a major significant factor for GHS/QOL decline at 3 months after treatment (per deficie

65 for FOLFIRINOX compared with gemcitabine for GHS, physical, role, cognitive, and social functioning,

66 sed to produce rats that were homozygous for GHS loci in the HC1 region between markers D1Mit2 and D1

67 In our search for GHS-R family members, we recently described the cloning

68 The genetic hypercalciuric stone-forming (GHS) rat is an animal model that closely resembles human

69 The genetic hypercalciuric stone-forming (GHS) rat model displays complex changes in physiology in

70 female genetic hypercalciuric stone-forming (GHS) rats (Rattus norvegicus) had higher coefficients of

71 ria in genetic hypercalciuric stone-forming (GHS) rats is accompanied by intestinal Ca hyperabsorptio

72 inbred genetic hypercalciuric stone-forming (GHS) rats is due, in part, to a decrease in renal tubule

73 termed genetic hypercalciuric stone-forming (GHS) rats.

74 us (QTL) mapping of rats that were bred from GHS female rats and normocalciuric Wistar Kyoto (WKY) ma

75 rat, an F2 generation of 156 rats bred from GHS female rats and normocalciuric WKY male rats was stu

76 ed in the sequence of duodenal VDR mRNA from GHS rats compared with wild-type animals.

77 is of extracts of renal cortical tissue from GHS and NC rats revealed a major 7-kb transcript of CaR

78 tigated the possible existence of functional GHS-R1a:GHS-R1b:D5R oligomeric complexes in the VTA.

79 The estimated affinity constants for GHR/GHS-R1a and antagonist/GHS-R1a in the absence of G prote

80 mely, the strong promoting effect on the GHR/GHS-R1a interaction at low molar ratios GHR/antagonist.

81 The antagonists potentiate the GHR/GHS-R1a interaction, and they display the same effect on

82 , different approaches to antagonize ghrelin/GHS-R1a signaling have been pursued for the treatment of

83 Disruption of the endogenous ghrelin/GHS-R pathway by RNA interference resulted in diminished

84 sed by pharmacological inhibition of ghrelin/GHS-R interaction.

85 indings suggest a novel role for the ghrelin/GHS-R axis in astrocytoma cell migration and invasivenes

86 guously demonstrated that in addition to Gq, GHS-R1a also promoted constitutive activation of G13.

87 e of peptides and non-peptides known to have GHS activity was used to generate and assess a 3D pharma

88 KRd patients had higher GHS/QoL scores versus Rd patients over 18 treatment cycl

89 However, GHS-R1a is expressed in other brain regions, including t

90 BACKGROUND & AIMS: Gastric hypersensitivity (GHS) contributes to epigastric pain in patients with fun

91 Gastric hypersensitivity (GHS) contributes to epigastric pain in patients with fun

92 s show decreased mRNA levels of hypothalamic GHS-R1a, neuropeptide Y (NPY), and agouti-related protei

93 9%) of 297 in the placebo group had improved GHS-QoL at any time during the study (p=0.0003).

94 emotherapy maintained GHS/QOL, with improved GHS/QOL scores at week 21 in the pembrolizumab plus chem

95 Conclusion KRd improves GHS/QoL without negatively affecting patient-reported sy

96 In GHS chromosome 1 congenic lines bred onto a WKY genomic

97 score-adjusted mean change from baseline in GHS was -3.40 (95% CI -7.82 to 1.03; p=0.13) in the radi

98 differences in mean changes from baseline in GHS/QoL, functioning, and symptoms per EORTC QLQ-C30 did

99 Mean change from baseline in GHS/QoL, overall cancer and prostate cancer-specific fun

100 Median time to true deterioration in GHS-QoL was not reached (NR; 95% CI 13.4 months-NR) in t

101 etermine the level of CaR gene expression in GHS rat kidney and whether CaR gene expression is regula

102 d renal CaR mRNA levels 2.0- and 3.3-fold in GHS and NC rats, respectively.

103 NC rats, CaR mRNA levels remained higher in GHS rat kidney, and the elevation was more sustained.

104 ncreased basal CaR mRNA expression levels in GHS rat kidney.

105 Under basal conditions, VDR mRNA levels in GHS rats were lower in duodenum and higher in kidney com

106 duodenal and renal calbindin mRNA levels in GHS rats, whereas they were either suppressed or unchang

107 mean changes from baseline were observed in GHS/QoL, symptom, and functional scales between the trea

108 ealed a four-fold increase in CaR protein in GHS rat renal tissue, and 1,25(OH)2D3 administration inc

109 creased VDR gene expression significantly in GHS but not normocalciuric animals, in a time- and dose-

110 In vivo half-life of VDR mRNA was similar in GHS and control rats in both duodenum and kidney, and wa

111 that D1R co-expression promotes a switch in GHS-R1a-G protein coupling from Gi/o to Gs/olf, but only

112 l interfering RNAs against K(v)1.1 increased GHS in naive rats.

113 ticosterone on post-natal day 15 and induced GHS in adult life.

114 y determines the efficacy of ghrelin-induced GHS-R1a-mediated signaling but also determines the abili

115 nsult to the colons of neonatal rats induced GHS in adult life.

116 nd high relative GHS-R1b expression inhibits GHS-R1a function by facilitating GHS-R1a trafficking to

117 ffect operates through a mechanism involving GHS-R1a.

118 ), is coexpressed with its truncated isoform GHS-R1b, which does not bind ghrelin or signal, but olig

119 ), and Global Health Status-Quality of Life (GHS-QoL) and physical function subscales of European Org

120 ion in global health status/quality of life (GHS/QoL) per European Organisation for Research and Trea

121 The Global Health Status/Quality of Life (GHS/QoL) scale and seven subscales (fatigue, nausea and

122 LQ-C30 global health status/quality of life (GHS/QOL) score, and time to deterioration in cough, ches

123 LQ-C30 global health status/quality of life (GHS/QOL) scores were maintained from baseline and were s

124 LQ-C30 global health status/quality of life (GHS/QOL), and -4.96 (0.85) versus -6.64 (0.94) for the E

125 -SF]); global health status/quality of life (GHS/QoL), overall cancer and prostate cancer-specific fu

126 LQ-C30 global health status/quality of life (GHS/QOL), physical functioning, social functioning, and

127 In the liver, GHS-R1a mRNA was expressed predominantly in cholangiocyt

128 olizumab to standard chemotherapy maintained GHS/QOL, with improved GHS/QOL scores at week 21 in the

129 Male GHS and normal control (NC) rats were fed a Ca-sufficien

130 ghrelin (AG) and UAG were abolished in male GHS-R-null mice.

131 (OH)2D3 may mediate these observations, male GHS and wild-type Sprague- Dawley normocalciuric control

132 eripheral GHS-R blockage with small molecule GHS-R antagonists might not be sufficient for suppressin

133 identified as a new class of small-molecule GHS-R1a antagonists.

134 Moreover, GHS-R1a activation enhances two different paradigms of l

135 rowth hormone secretagogue receptor, namely, GHS-R1a.

136 outer walls of graphene hollow nanospheres (GHSs), realizing separate-sided different single-atom fu

137 lore chemical structures that could be novel GHSs.

138 signaling but also determines the ability of GHS-R1a to form oligomeric complexes with other receptor

139 ent upon acylation by GOAT and activation of GHS-R.

140 Reducing the ligand-independent activity of GHS-R1a increased the surface diffusion of AMPA receptor

141 re we examined pharmacological antagonism of GHS-R in motivational incentive learning, as reflected i

142 At concentrations of GHS-R1a and SST5 expressed in islets, time-resolved FRET

143 fulvestrant delayed time to deterioration of GHS/QOL and maintained other dimensions of HRQOL (except

144 Median time to definitive deterioration of GHS/QoL was longer in the talazoparib plus enzalutamide

145 )]-ghrelin), has enabled the distribution of GHS-R receptor protein to be directly demonstrated.

146 In this study, we examined the effect of GHS in immunological functions of 5- to 6-wk-old and 16-

147 Here we report the effects of GHS-R antagonists, some of which were potent, selective,

148 Differential co-expression of GHS-R1a and GHS-R1b, both in HEK-293T cells and in stria

149 /o to Gs/olf, but only upon co-expression of GHS-R1b.

150 assays illustrate constitutive formation of GHS-R1a:SST5 heteromers in which ghrelin, but not SST, s

151 -R1a-G-protein coupling and the formation of GHS-R1a:SST5 heteromers is dependent on the ratio of ghr

152 ese results suggest dissociable functions of GHS-R in its influence over motivational learning and in

153 This hyperresponsiveness of GHS rats to 1,25(OH)2D3 (a) occurs through an increase i

154 ter neonatal insult blocked the induction of GHS in adult rats.

155 isplay the same effect on the interaction of GHS-R1a with other agonists listed as doping agents.

156 s 6-, 11-, 15-, and 29-fold higher levels of GHS-R compared with primary normal human astrocytes.

157 The ligation of GHS-R by ghrelin on these cells resulted in an increase

158 approaches to investigate the mechanisms of GHS in adult rats subjected to neonatal colonic insult b

159 tes that GHS-R1b acts as a dual modulator of GHS-R1a function: low relative GHS-R1b expression potent

160 GHS-R1b also facilitates oligomerization of GHS-R1a with D1R, conferring GHS-R1a distinctive pharmac

161 previously reported distribution pattern of GHS-R mRNA.

162 ly be determined from expression patterns of GHS-R mRNA or the use of immunohistochemical techniques

163 ts with GHS-R1a, but only in the presence of GHS-R1b.

164 provides evidence for a predominant role of GHS-R1a:GHS-R1b:D1R oligomers in rodent VTA as main medi

165 provided evidence for a predominant role of GHS-R1a:GHS-R1b:D1R oligomers in the rodent VTA as main

166 we reveal a more complex modulatory role of GHS-R1b.

167 ate a hyperphagic response to stimulation of GHS-R in the caudal brainstem.

168 ies were found to be different from those of GHS-R1a:GHS-R1b:D1R oligomers, including weak Gs couplin

169 by exerting a negative allosteric effect on GHS-R1a signaling, respectively.

170 ay crystal structure of DHFR docked with our GHS-R antagonists and GHS-R modeling, we designed and sy

171 Overall, GHS and quality of life were maintained for both treatme

172 n, whereas tumor cells stably overexpressing GHS-R exhibited increased cell motility.

173 elin actions with ghrelin antibody, peptidyl GHS-R antagonists, and antisense oligonucleosides result

174 onstrated for the first time that peripheral GHS-R blockage with small molecule GHS-R antagonists mig

175 ntages of responders with >/= 5- or 15-point GHS/QoL improvement at each cycle were compared between

176 ry and synthesis of a novel series of potent GHSs, a number of which had nanomolar in vitro activity.

177 e activity, we have reconstituted a purified GHS-R1a monomer in a lipid disc.

178 requirements for the interaction of purified GHS-R1a with arrestin and AP2 provide a new rationale to

179 a preferential Gi/o coupling of the GHS-R1a-GHS-R1b complex in HEK-293T cells and, unexpectedly, a p

180 s evidence for a predominant role of GHS-R1a:GHS-R1b:D1R oligomers in rodent VTA as main mediators of

181 d evidence for a predominant role of GHS-R1a:GHS-R1b:D1R oligomers in the rodent VTA as main mediator

182 found to be different from those of GHS-R1a:GHS-R1b:D1R oligomers, including weak Gs coupling and th

183 the possible existence of functional GHS-R1a:GHS-R1b:D5R oligomeric complexes in the VTA.

184 GHS-R1a:GHS-R1b:D5R oligomers were first demonstrated in mammali

185 in receptor growth hormone secretagogue R1b (GHS-R1b) has been suggested to simply exert a dominant n

186 The G protein-coupled receptor GHS-R1a mediates ghrelin-induced growth hormone secretio

187 d both are mediated through ghrelin receptor GHS-R.

188 In this context, ghrelin receptor GHS-R1a is a peculiar receptor in the sense that it disp

189 of the full and functional ghrelin receptor GHS-R1a.

190 le to activate the cognate ghrelin receptor (GHS-R), unacylated ghrelin (UAG) possesses a unique acti

191 nd inverse agonists of the ghrelin receptor (GHS-R1a) are widely considered to offer utility as antio

192 ptors (GPCRs), such as the ghrelin receptor (GHS-R1a), the melanocortin 3 receptor (MC(3)), and the s

193 t accommodate noncanonical ghrelin receptor (GHS-R1a)-G-protein coupling to Galpha(i/o) instead of Ga

194 ilable growth hormone secretagogue receptor (GHS-R) antagonists are reported.

195 xamide growth hormone secretagogue receptor (GHS-R) antagonists were discovered.

196 g of a growth hormone secretagogue receptor (GHS-R) from human pituitary gland and brain identified a

197 eptor (growth hormone secretagogue receptor (GHS-R)) are widely expressed in a number of organ system

198 ceptor Growth Hormone Secretagogue Receptor (GHS-R), but the physiologically relevant receptor of obe

199 r, the growth hormone secretagogue receptor (GHS-R), in the caudal brainstem.

200 or the growth hormone secretagogue receptor (GHS-R), is produced by stomach cells and is a potent cir

201 or the growth hormone secretagogue receptor (GHS-R).

202 of the growth hormone secretagogue receptor (GHS-R).

203 ype 1a growth hormone secretagogue receptor (GHS-R1a) and the only currently known circulating appeti

204 ion of growth hormone secretagogue receptor (GHS-R1a) antagonists in urine samples.

205 own as growth hormone secretagogue receptor (GHS-R1a), is coexpressed with its truncated isoform GHS-

206 us via growth hormone secretagogue receptor (GHS-R1a).

207 ng at growth hormone secretagogue receptors (GHS-R), the only sites of action for this gastric hormon

208 5-HT(2C)-VSV isoform, significantly reduced GHS-R1a agonist-mediated calcium influx, which was compl

209 R1b expression potentiates and high relative GHS-R1b expression inhibits GHS-R1a function by facilita

210 modulator of GHS-R1a function: low relative GHS-R1b expression potentiates and high relative GHS-R1b

211 are consistent with physiologically relevant GHS-R1a:SST5 heteromerization that explains differential

212 stabilizes heteromer conformation, restoring GHS-R1a-Galpha(q11) coupling.

213 cDNA clone was identified encoding a second GHS-R-related gene (GPR39).

214 effects of an orally active GH secretagogue (GHS) treatment that causes a release of endogenous GH on

215 idyl small m.w. compound, a GH secretagogue (GHS), was found to induce the production of GH by the pi

216 ligand for the growth hormone secretagogue (GHS) receptor, yielded the surprising result that the pr

217 st of the human growth hormone secretagogue (GHS) receptor.

218 relin mRNAs and growth hormone secretagogue (GHS) receptors could be detected in human oral epithelia

219 ered as a human growth hormone secretagogue (GHS).

220 Growth hormone secretagogues (GHS) are a group of synthetic peptide and nonpeptide mol

221 lecules termed growth hormone secretagogues (GHSs) act on the pituitary gland and the hypothalamus to

222 al entities as growth hormone secretagogues (GHSs), a small database of peptides and non-peptides kno

223 esized a series of potent and DHFR selective GHS-R antagonists with good pharmacokinetic (PK) profile

224 Over the years, several GHS-R1a ligands have been identified and some of them ha

225 with GH-releasing hormone and somatostatin, GHS receptors have also been identified on hypothalamic

226 Besides, we identified some GHS-R1a ligands that preferentially activated Gq and ant

227 se differences are linked to ligand-specific GHS-R1a conformations, as assessed by intrinsic fluoresc

228 EORTC QLQ-C30 baseline global health status (GHS) scores for T-DXd (n = 253) and T-DM1 (n = 260) were

229 Baseline EORTC QLQ-C30 global health status (GHS) scores were similar with trastuzumab deruxtecan (n=

230 mean changes for EORTC global health status (GHS) were +10.1 (95% CI 7.0 to 13.1) and -1.5 (95% CI -5

231 om baseline in QLQ-C30 global health status (GHS)-quality of life (QoL) was a prespecified secondary

232 hange in EORTC QLQ-C30 Global Health Status (GHS)/QOL from baseline up to week 26 favoured enfortumab

233 sk of deterioration in global health status (GHS)/quality of life (QoL) (hazard ratio 0.54).

234 change in the QLQ-C30 global health status (GHS)/quality-of-life (QOL) score and time to deteriorati

235 Improvement in global health status (GHS; P < .001) was observed in the FOLFIRINOX arm and im

236 ating the involvement of D1R in the striatal GHS-R1a-Gs/olf coupling.

237 tumor tissue microarray revealed that strong GHS-R and ghrelin expression was significantly more comm

238 lysis was based on a Gutenberg Health Study (GHS) cohort that included 4335 eligible enrollees from a

239 The Gutenberg Health Study (GHS) is a population-based, observational cohort study.

240 Study [FHS; n=2992], Gutenberg Health Study [GHS; n=4354], and Multinational Monitoring of Trends and

241 Hydroxyproline-supplemented GHS rats were used to test the hypothesis that the thiaz

242 urotrophic factor in FD-like rats suppressed GHS.

243 n (CVs) for urinary calcium (CV = 0.14) than GHS males (CV = 0.06), and the reverse in normocalciuric

244 These results demonstrate that GHS rats have high levels of CaR gene expression and CaR

245 campal neurons in culture, demonstrates that GHS-R1b acts as a dual modulator of GHS-R1a function: lo

246 We have also found that GHS promoted better thymic engraftment in bone marrow tr

247 We propose that GHS-R1a activation in the hippocampus enhances excitator

248 Here we report that GHS-R and ghrelin are expressed in human T lymphocytes a

249 We show that GHS-R1a coupling to Galpha(i/o) rather than Galpha(q11)

250 Our data show that GHS-R1a is localized in the vicinity of hippocampal exci

251 Previous studies showed that GHS-R1b also facilitates oligomerization of GHS-R1a with

252 The results suggest that GHS rats hyperrespond to minimal doses of 1,25(OH)2D3 by

253 nhanced in the treated mice, suggesting that GHS has a considerable immune enhancing effect, particul

254 the spleens of treated mice, suggesting that GHS may exert its immune enhancing effect by promoting c

255 This unique characteristic suggests that GHS rats may be susceptible to minimal fluctuations in s

256 eight-fold phenotypic difference between the GHS and WKY progenitors were mapped.

257 In addition, a novel heterodimer between the GHS-R1a receptor and the 5-HT(2C) receptor was identifie

258 with moderate sequence identity to both the GHS-R and neurotensin-R.

259 mosomes, distinct from the gene encoding the GHS-R and NT-R type 1.

260 xcretion was six- to eightfold higher in the GHS female than in the WKY male progenitors.

261 In the GHS group, LV fractional shortening was higher (29+/-2%)

262 oci that contribute to hypercalciuria in the GHS rat, an F2 generation of 156 rats bred from GHS fema

263 A higher proportion of KRd patients met the GHS/QoL responder definition (>/= 5-point improvement) w

264 serve the calcium excretion phenotype of the GHS parent strain.

265 recursor, hydroxyproline, to the diet of the GHS rats leads to formation of calcium oxalate (CaOx) ki

266 (200 nmol) intraperitoneal injections of the GHS-R antagonist GHRP-6 [D-Lys3] prior to subsequent tra

267 ential for the binding and activation of the GHS-R by structurally dissimilar GHSs, was conserved in

268 The nucleotide sequence of the GHS-R is most closely related to the neurotensin recepto

269 Superfusion of the GHS-R1A antagonists D-Lys3-GHRP-6 and JMV 3002 decreased

270 the future pharmacological targeting of the GHS-R1a receptor in the homeostatic regulation of energy

271 activity via promiscuous dimerization of the GHS-R1a receptor with other G protein-coupled receptors

272 lization following heterodimerization of the GHS-R1a receptor with the dopamine 1 receptor, as well a

273 Interestingly, dimerization of the GHS-R1a receptor with the unedited 5-HT(2C)-INI receptor

274 We found a preferential Gi/o coupling of the GHS-R1a-GHS-R1b complex in HEK-293T cells and, unexpecte

275 dopamine 1 receptor, as well as that of the GHS-R1a-MC(3) heterodimer.

276 ovel G-protein-coupled receptor (GPC-R), the GHS-R.

277 6 analogues with reduced affinity toward the GHS-R1a by at least a factor of 100 and in certain cases

278 36 receptor with reduced affinity toward the GHS-R1a.

279 ficant amino acid sequence identity with the GHS-R and NT-Rs 1 and 2.

280 cloned and was shown to be the target of the GHSs.

281 GH release and supports the notion that the GHSs mimic an undiscovered hormone.

282 Therefore, GHS-R1b not only determines the efficacy of ghrelin-indu

283 Accordingly, we found that blocking this GHS-R1a activity impaired spatial and recognition memory

284 bestatin regulates insulin secretion through GHS-R.

285 These observations ascribe to GHS a novel therapy possible for aging, AIDS, and transp

286 inum-based chemotherapy without detriment to GHS/QOL, pain, or functioning.

287 ry insult to the colons of rat pups leads to GHS in adult life.

288 a potential novel mechanism for fine-tuning GHS-R1a receptor-mediated activity via promiscuous dimer

289 ytokine expression, while leptin upregulated GHS-R expression on human T lymphocytes.

290 ntake in mice, and it was demonstrated using GHS-R1a null and wild-type mice that this effect operate

291 ocytes and monocytes, where ghrelin acts via GHS-R to specifically inhibit the expression of proinfla

292 , regulating cholangiocyte proliferation via GHS-R1a, a G-protein coupled receptor which causes incre

293 duced GSIS was absent in beta-cells in which GHS-R was suppressed.

294 With GHS treatment, the ratio of LV mass to body weight incre

295 ating the different pathways associated with GHS-R1a in HEK293T cells.

296 r experiments showed that D1R interacts with GHS-R1a, but only in the presence of GHS-R1b.

297 improved LV pump function that occurred with GHS treatment in this model of CHF was most likely a res

298 ind ghrelin or signal, but oligomerizes with GHS-R1a, exerting a complex modulatory role that depends

299 o-localization of the small GTPase Rac1 with GHS-R on the leading edge of the astrocytoma cells and i

300 The old mice, treated with GHS for 3 wk, did not show increases in peripheral lymph

301 raised the potential interaction of UAG with GHS-R in the regulation of bone marrow adiposity.

302 nd was increased from pacing CHF values with GHS treatment (55+/-7 microm/s, P:<0.05).