ライフサイエンスコーパス: G-protein coupling

1 ues of the G alpha s protein in the receptor/G protein coupling.

2 e in GPCR activation and productive receptor/G protein coupling.

3 treatment with GTPgammaS was used to inhibit G protein coupling.

4 possible role for CaM in regulating receptor-G protein coupling.

5 n-dependent pathway, which is independent of G protein coupling.

6 gation, (iv) microswitch activation, and (v) G protein coupling.

7 nsmembrane domains in ligand recognition and G protein coupling.

8 ivity and reduced the efficiency of receptor/G protein coupling.

9 roles in receptor activation and/or receptor/G protein coupling.

10 rimeric G proteins are required for receptor-G protein coupling.

11 ing to arrestin association which interdicts G protein coupling.

12 RK currents occur at a critical threshold of G protein coupling.

13 used by an increase in intrinsic efficacy of G protein coupling.

14 that dimerization may be a prerequisite for G protein coupling.

15 ts of membrane lipid composition on receptor-G protein coupling.

16 a(2+) channels, but lacked voltage-dependent G protein coupling.

17 f alpha(2B)AR but not functional alpha(2B)AR-G protein coupling.

18 cannabinoid receptor 1 (CB1) and antagonized G protein coupling.

19 class II receptors are the likely sites for G protein coupling.

20 i3 near TM helices 5 and 6 were required for G protein coupling.

21 tor (AT(1)-R) is an important determinant of G protein coupling.

22 argets for modulation of agonist binding and G protein coupling.

23 could have a significant impact on receptor-G protein coupling.

24 had distinct kinetic properties in receptor-G protein coupling.

25 vation of G(i) but not required for receptor-G protein coupling.

26 anced agonist potency, binding affinity, and G protein coupling.

27 anthosine 5'-triphosphate (XTP)] on receptor/G protein coupling.

28 of Ang II may reflect a selective effect on G protein coupling.

29 in complex and, as the result, the extent of G protein coupling.

30 tors, apparently due to promiscuous receptor/G protein coupling.

31 tion about mechanisms of signal transfer and G protein coupling.

32 cating an inhibitory site distal to receptor/G protein coupling.

33 e study of factors that control V1a receptor/G protein coupling.

34 but plays a novel role in regulating 5-HT2AR G protein coupling.

35 t mediated by changes in receptor density or G protein coupling.

36 t to a critical role for Lys-319 in receptor-G protein coupling.

37 e wild type m2 receptor completely abolished G protein coupling.

38 relationships in terms of ligand-binding and G protein coupling.

39 of PAR1 surface expression and efficiency of G protein coupling.

40 ty of H8 are critical for efficient receptor-G protein coupling.

41 cts the conformational changes necessary for G protein coupling.

42 binding to CB1 yet acts as an antagonist of G protein coupling.

43 r ligand-binding and GBR2 is responsible for G protein coupling.

44 c receptor (betaAR, a GPCR) complex altering G protein coupling.

45 is structurally homologous but deficient in G protein coupling.

46 changing ligand binding affinity or receptor-G protein coupling.

47 tracellular loop also demonstrated broadened G protein coupling.

48 g, stability, (125)I-CXCL12 degradation, and G protein-coupling.

49 an intracellular binding site that enhances G-protein coupling.

50 outward helical movement of TM6 required for G-protein coupling.

51 (arrestins), which prevents further receptor-G-protein coupling.

52 whether ERK activation differs according to G-protein coupling.

53 omain of CXCR4, or pertussis toxin-sensitive G-protein coupling.

54 , with a corresponding reduction in receptor/G-protein coupling.

55 relationships of each of these residues for G-protein coupling.

56 he i3 loop of m5 (Ni3) that are critical for G-protein coupling.

57 ts were caused primarily by changes receptor/G-protein coupling.

58 m5 muscarinic receptor as being critical for G-protein coupling.

59 ntified where mutations compromised receptor/G-protein coupling.

60 etylcholine receptor for domains that govern G-protein coupling.

61 els that incorporate receptor activation and G-protein coupling.

62 lar loops of receptors play pivotal roles in G-protein coupling.

63 ic side chain of residue 217 participates in G-protein coupling.

64 IP signal originate and diverge upstream of G-protein coupling.

65 is loop are sufficient to direct appropriate G-protein coupling.

66 on adenylyl cyclase because of differential G-protein coupling.

67 like mGluR2, a single 7TM is sufficient for G-protein coupling.

68 igand binding and the efficiency of receptor G-protein coupling.

69 xerting allosteric antagonism and preventing G-protein coupling.

70 ated the allosteric effect on CRF-stimulated G-protein coupling.

71 el motifs associated with ligand binding and G-protein-coupling.

72 neuron MOR and a reduction in functional MOR G-protein-coupling.

73 l GEF/Ras pathway but separate receptors and G protein couplings.

74 ble with SR141716A in antagonizing the basal G protein coupling activity of CB1, as indicated by a re

75 In contrast basal G protein coupling activity of the three variants was un

76 istinct regions critical for ligand binding, G protein coupling activity, and receptor trafficking.

77 the receptor-Gi interface resulted in little G protein coupling activity, consistent with the present

78 t CP55,940 while exhibiting an antagonism of G-protein coupling activity.

79 ein coupling), and CAM alpha(2A)AR (enhanced G protein coupling) all exhibited a cell surface alpha(2

80 -arrestin binding, which terminates receptor-G protein coupling, also initiates a second wave of sign

81 develop KOR agonists that are biased toward G protein coupling and away from betaarrestin2 recruitme

82 Agonists at KOR can promote G protein coupling and betaarrestin2 recruitment as well

83 tor phosphorylation at the level of receptor/G protein coupling and by an unknown mechanism at the le

84 - and S268P-MOR, suggesting that domains for G protein coupling and CaM binding overlap partially.

85 s bound secretin normally, leading to normal G protein coupling and cAMP accumulation and prompt rece

86 ediated signaling by increasing both beta2AR-G protein coupling and intrinsic adenylyl cyclase activi

87 rotein-coupled receptors, thereby preventing G protein coupling and often switching signaling to othe

88 argeting regions of the receptor involved in G protein coupling and phosphorylation.

89 AT1R occurs independently of heterotrimeric G protein coupling and, if so, the cellular function of

90 The aim of this study was to investigate the G protein-coupling and -signaling properties of the edg-

91 n-coupled receptors (GPCRs) is important for G protein-coupling and activation; in addition, sorting

92 ased receptor with intact ligand binding and G-protein coupling and activation, but deficient in rece

93 mice was investigated in terms of beta(3)AR-G-protein coupling and adenylyl cyclase activation.

94 plications for the stoichiometry of receptor-G-protein coupling and cross talk in signaling pathways.

95 ich was accompanied by defective D1 receptor G-protein coupling and loss of natriuretic response to S

96 ess, normalized BP, and restored D1 receptor G-protein coupling and natriuretic response to SKF38393.

97 ate receptor signaling by impairing receptor-G-protein coupling and promoting receptor internalizatio

98 by 2 distinct PDZ proteins via modulation of G-protein coupling and receptor signaling.

99 GHS-R1a-G-protein coupling and the formation of GHS-R1a:SST5 het

100 R314, at the distal end of ICL3, impaired G-protein coupling and to a lesser extent reduced CGRP a

101 sociated with beta-arrestin-2 recruitment or G-protein coupling and validate relevance of the design

102 racellular loop), D79N alpha(2A)AR (impaired G protein coupling), and CAM alpha(2A)AR (enhanced G pro

103 of MOP signaling: receptor internalization, G protein coupling, and activation of extracellular sign

104 e GnRH-induced inositol phosphate signaling, G protein coupling, and agonist-induced internalization

105 fluences the ligand-uptake/degradation rate, G protein coupling, and receptor stability.

106 ayed similar ligand binding characteristics, G protein coupling, and signal transduction as their res

107 binds to the AT(1)R, reduces heterotrimeric G-protein coupling, and inhibits IP(3) (inositol-1,4,5-t

108 rmal ligand binding affinity, markedly lower G-protein coupling, and markedly lower chemotaxis toward

109 of FPR, their ligand binding affinity, their G-protein coupling, and their chemotaxis toward N-formyl

110 ed ( approximately 50% reduction in receptor-G-protein coupling, as compared to control M3R).

111 gous, involving changes in the efficiency of G-protein coupling, as there were parallel decreases in

112 formational change that exposes a domain for G protein coupling at the cytosolic surface of the helic

113 cond loop mutant, which lacks heterotrimeric G protein coupling (AT1a-i2m).

114 e as G(i) activators rather than in receptor-G protein coupling, because high-affinity agonist bindin

115 The G protein coupling behavior of four human 5-hydroxytrypt

116 ed 5-HT1 receptor subtypes exhibit different G protein coupling behaviors.

117 ity agonist binding as a measure of receptor-G protein coupling, betagamma-containing gamma11 was the

118 showed that JF5 was selective with regard to G protein coupling, blocking signaling mediated by G(alp

119 portant for the affinity of ligand-dependent G protein coupling but did not affect the maximal signal

120 gonist, the biased ligand (R)-4 induced poor G protein coupling but substantial beta-arrestin recruit

121 f biased KOR agonists that potently activate G protein coupling but weakly recruit betaarrestin2.

122 receptors, mGluR1 and mGluR5, occurs through G-protein coupling, but evidence suggests they might als

123 Here we explore specificity in receptor-G protein coupling by taking advantage of the ability of

124 okines and opioids tested was able to induce G protein coupling by U51, and no evidence for opioid li

125 p of MOR caused substantial changes in basal G protein coupling, CaM binding, or both.

126 f9 insect cells exhibited ligand binding and G-protein coupling characteristics similar to the wild-t

127 ficking to the cell surface, ligand binding, G protein coupling, chronic desensitization, and down-re

128 examining the ability of ligand binding- and G protein coupling-defective alpha-factor receptors to f

129 Co-expression of ligand binding- and G protein coupling-defective mutant receptors did not si

130 ection from an inherent instability of these G protein coupling-defective receptors.

131 ed upon coexpression with wild-type, but not G protein coupling-defective, receptors.

132 to require G-proteins as it was seen in two G-protein coupling-defective GIRK mutants and in excised

133 3 cells, both the native AT1a receptor and a G protein-coupling deficient DRY/AAY mutant recruited be

134 60 min compared with 76-87% for WT, loss of G protein coupling did not account for differences in in

135 However, treatment with GTPgammaS to inhibit G protein coupling diminished the affinity change for th

136 gic receptor is bound to a full agonist, the G protein coupling domain exists in two distinct conform

137 oduction of a Y690V mutation in the putative G protein-coupling domain of R2 is sufficient to confer

138 ligand-induced conformational changes in the G protein-coupling domain of the beta(2) adrenergic rece

139 nergic receptor (beta(2)AR), adjacent to the G-protein-coupling domain.

140 to be in close proximity where they form the G-protein-coupling domain.

141 In our effort to identify G protein coupling domains of the human platelet ADP rec

142 ting that this domain mimics the function of G-protein-coupling domains found in receptors.

143 in the transmembrane core to the cytoplasmic G-protein-coupling domains.

144 of the mu-opioid receptor regulates receptor-G protein coupling efficacy.

145 native tissues leads to an enhanced receptor/G protein coupling efficiency that contributes to sensit

146 the DRY motif may reduce mu-opioid receptor-G-protein coupling efficiency.

147 s in receptor structure which alter receptor-G protein coupling (either an increase or decrease) are

148 Thus, novel G protein coupling enables a subpopulation of ERalpha to

149 In class A GPCRs, receptor activation and G-protein coupling entail outward movements of transmemb

150 ired arginine vasopressin-dependent receptor/G protein coupling for cell growth.

151 We found increased G protein coupling for delta opioid receptor (DOR) and m

152 We discovered that the specific activity of G protein coupling for single rhos sequestered in indivi

153 This reduced G protein coupling for the edited isoforms is primarily

154 and heteromer formation leads to a switch in G-protein coupling for 5-HT2AR from Gq to Gi proteins.

155 Little is known about the events prior to G-protein coupling: for example, whether these signals a

156 R co-expression promotes a switch in GHS-R1a-G protein coupling from Gi/o to Gs/olf, but only upon co

157 the use of more direct measures of receptor-G protein coupling (GTPase activity, GTP gamma S binding

158 terminants governing the selectivity of GPCR/G protein coupling, however, remain obscure.

159 s of spontaneous and ligand-induced receptor-G protein coupling in delta (DOP) and mu (MOP) opioid re

160 amino acids and may therefore underlie GPCR/G protein coupling in general.

161 utively activates the receptor, resulting in G protein coupling in the absence of agonist and activat

162 point to experience-specific shifts in PAR1-G protein coupling in the amygdala as a novel mechanism

163 Although the CXCR7 C terminus abolished G protein coupling in the CXCR4-7tail mutant, replacemen

164 These findings implicate abnormal betaAR-G protein coupling in the pathogenesis of the failing he

165 the specific binding of A1-AdoR and A1-AdoR/G protein coupling in ventricular myocardium of 6- to 24

166 ors and influence the efficiency of receptor-G protein coupling in vitro.

167 mutation abolished agonist-induced receptor/G protein coupling in yeast.

168 Nlxz infusion prevented DAMGO stimulation of G-protein coupling in LPBNi and markedly reduced this st

169 l (i.t.) morphine administration on receptor/G-protein coupling in the spinal cord.

170 inositol phosphate production (a measure of G-protein coupling) in association with mutational analy

171 mportantly, our results indicate a switch in G-protein coupling, in which E775K loses G(o) coupling b

172 severely reduced the efficiency of receptor/G protein coupling, indicating that the targeted residue

173 n attenuated the desensitization of receptor G-protein coupling induced by phorbol 12-myristate.

174 triphosphate binding, which is indicative of G protein coupling inhibition in a concentration-depende

175 g between the agonist-binding pocket and the G-protein-coupling interface (TM5 and TM6), similar to t

176 ric coupling of the agonist-binding site and G-protein-coupling interface that may generally be respo

177 end of transmembrane domain (TM) 4, whereas G protein coupling involves ic1, ic3, the C-terminal tai

178 s the anterior cingulate cortex: D1 receptor-G protein coupling is greatly reduced, the GABAergic sys

179 st that GRK-mediated termination of receptor-G protein coupling is likely to regulate synaptic streng

180 q and G11 (Fq/11 cells) to determine whether G protein coupling is necessary for agonist-dependent re

181 e important link between agonist binding and G protein coupling is not known.

182 d in this interaction, and that alpha(1B)-AR G protein coupling is not required.

183 Because G protein coupling is reported to have a selective effec

184 In contrast, 5-HT(1A) receptor levels and G-protein coupling is normal in Tph2 knockin mice, indic

185 MOPr induces receptor desensitization at the G protein coupling level.

186 ontacts from the retinal binding site to the G protein-coupling loops.

187 ess that likely represents interference with G protein coupling, manifest as a reduced rate of cAMP s

188 This suggests that G-protein coupling may be a novel sugar-signaling mechan

189 e-binding protein (denoted BBP) containing a G protein-coupling module.

190 flects the in vivo stoichiometry of receptor/G-protein coupling more closely than was previously assu

191 on the same face of an alpha helix, formed a G-protein coupling motif.

192 potential to correct the defective receptor-G protein coupling observed in the high membrane cholest

193 at homologous desensitization of mu receptor/G-protein coupling occurs specifically in spinal cord fo

194 We examined the expression, binding, and G protein coupling of 28 mutated forms of FPR in stably

195 injections of fluoxetine on the density and G protein coupling of 5-HT1A receptors in hypothalamic n

196 the structure of the receptor interface for G protein coupling of a PAFR and suggests a conserved ro

197 for their capacity to sterically hinder the G protein coupling of agonist-activated seven-transmembr

198 l disruption of its amphipathic character on G protein coupling of and signaling by the rPAFR.

199 G protein coupling of GPR40 was examined in Chinese hams

200 s a conserved role of amphipathic helices in G protein coupling of receptors ranging from those for b

201 Previous results have failed to show G protein coupling of the AT2 receptor in the fetus.

202 Morphine stimulated G protein coupling of the three receptor variants to a m

203 ne pretreatment significantly enhanced basal G protein coupling of wild type MOR, which is thought to

204 gest that fluoxetine gradually increases the G-protein coupling of 5-HT2A/2C receptors without alteri

205 significantly affected by the pH of binding, G-protein coupling of CCR5, or partial gp120 deglycosyla

206 etylcholine-stimulated increases in receptor-G-protein coupling of M(3)-AChR-N514Y reached only 12% o

207 on PTHrP production are because of alternate G-protein coupling of the receptor in normal versus tran

208 other G protein-coupled receptors, in which G protein coupling or phosphorylation are critical for l

209 tion may modulate the efficiency of receptor-G protein coupling or promote activation of Gbetagamma e

210 To determine whether functional receptor-G protein coupling or signaling are required for interna

211 lished upon treatment with agents that block G-protein coupling or deglycosylate the receptor.

212 affecting ligand binding affinity, receptor-G protein coupling, or U50,488H-induced desensitization

213 n animal by a dynamic shift between distinct G protein-coupling partners.

214 d water intake is mediated via the classical G protein coupling pathway, whereas the saline intake ca

215 se that the third intracellular loop forms a G-protein coupling pocket comprised of a positively char

216 lfills a structural role forming part of the G-protein coupling pocket, and that A441 contributes to

217 ructural role, forming the foundation of the G-protein-coupling pocket, whereas Tyr217 and Arg223 con

218 conformations that are independent of their G protein-coupling potency: one that allows the efficien

219 omology, they show pronounced differences in G-protein coupling preference and the physiological resp

220 superior cervical ganglion (SCG), the mGluR2/G protein coupling profile was characterized by reconsti

221 These findings suggest that the differential G protein coupling profiles of individual members of a s

222 s (GalRs) have been recently cloned, but the G protein coupling profiles of these receptors are not c

223 the two designer receptors differed in their G protein-coupling properties (G(q/11) versus G(s)).

224 nd an assessment of their ligand-binding and G protein-coupling properties.

225 ting multiple receptor isoforms with altered G-protein coupling properties.

226 Activation of FFA1 (GPR40), a member of G protein-coupling receptor family A, is mediated by med

227 nt efficacies were not due to differences in G-protein coupling, receptor desensitization, or recycli

228 n the gene encoding the alpha subunit of the G protein-coupling receptors to stimulation of adenylyl

229 ssion from the chemokine-binding site to the G protein-coupling region we engineered metal ion-bindin

230 In this study, we have mutated two putative G protein-coupling regions of CXCR2 and characterized th

231 o evidence of any quantitative difference in G protein coupling related to the number of hexadecapept

232 ate, mechanisms of signal initiation and FZD-G protein coupling remain poorly understood.

233 The G protein coupling requires the transmembrane domain of

234 sidues on the extracellular side of CXCR4 to G protein-coupling residues on its intracellular side.

235 than normal binding affinity, markedly lower G-protein coupling response, and markedly lower chemotax

236 affects the third loop and is defective for G-protein coupling retained the ability to undergo the a

237 sn(191) might be responsible for the altered G protein coupling seen with complete enzymatic deglycos

238 ammalian GPCR subfamily displaying different G-protein coupling selectivities.

239 ology to study mechanisms governing receptor/G protein coupling selectivity and receptor folding.

240 icating that the V2 receptor retained proper G protein coupling selectivity in yeast.

241 n of TM VI play key roles in determining the G protein coupling selectivity of the M(3) receptor subt

242 The molecular basis of receptor/G protein coupling selectivity was studied by using the

243 receptor had pronounced effects on receptor/G protein coupling selectivity.

244 cular mechanisms regulating peptide receptor/G protein coupling selectivity.

245 algorithm, capable of accurately predicting G-protein coupling selectivity, indicated that both huma

246 at residue motions in the ligand-binding and G-protein-coupling sites of the apo receptor are correla

247 approach was successful in the prediction of G protein coupling specificity of unknown sequences.

248 ns, the C-terminal ends of MCP-1Rs determine G protein coupling specificity.

249 restricted HMM based method to predict GPCR-G-protein coupling specificity has an error rate of <1%,

250 ilable in silico methods for predicting GPCR-G-protein coupling specificity have high error rate.

251 lar loop 1 and/or helix 8 may be involved in G-protein coupling specificity, as has been suggested fo

252 en applied to a test set of GPCRs with known G-protein coupling specificity.

253 te vicinity of a nonvisual GPCR modulate the G-protein-coupling step.

254 d characterized for functions in addition to G protein coupling, such as receptor phosphorylation and

255 hibited by approximately 50%, despite normal G protein coupling, suggesting a distal inhibitory locus

256 6N, R201A, and R205A also appeared to affect G protein coupling, suggesting that these residues may a

257 k between the agonist-binding pocket and the G-protein-coupling surface is not rigid.

258 phosphorylated active receptors, terminating G protein coupling, targeting receptors to endocytic ves

259 le reaction by associating with a regulatory G protein, coupling the energy of GTP hydrolysis to APS

260 ivated by Ang II even without heterotrimeric G protein coupling, the carboxyl terminus of the AT1 rec

261 questions about the specificity of receptor:G protein coupling, the regulation of cAMP formation in

262 ere additive contributions of Ni3 and Ci3 to G-protein coupling, the functional responses of two doub

263 Q mutant) did not alter receptor affinity or G protein coupling; therefore, it could be speculated th

264 Similarly, the degree of G protein coupling to 5-HT1A receptors varied markedly a

265 ave previously been shown to be critical for G protein coupling to many other G protein-coupled recep

266 ions have precluded a definitive analysis of G protein coupling to monomeric GPCRs in a biochemically

267 hod will allow molecular characterization of G protein coupling to other heptahelical receptors.

268 n but requires activation of PKC alpha after G protein coupling to phospholipase C.

269 e taste receptors or interfere with receptor-G protein coupling to serve as naturally occurring taste

270 rated that P4pal-10 selectively inhibits all G protein coupling to several Gq-coupled receptors, incl

271 n AngII analog that induces betaarr, but not G protein coupling to the AT(1)R, recapitulates the effe

272 to recover point mutations that can restore G protein coupling to the D113N mutant receptor.

273 i3) subunits, are indicative of differential G protein coupling to the LHR.

274 led receptor conformational dynamics control G protein coupling to trigger signaling is a key but sti

275 G-protein coupling to 5-HT(1A) receptors and G-protein l

276 Finally, alterations in G-protein coupling to 5-HT(1A) receptors are unlikely to

277 date noncanonical ghrelin receptor (GHS-R1a)-G-protein coupling to Galpha(i/o) instead of Galpha(q11)

278 nonetheless antagonized the agonist-induced G-protein coupling to the CB1 receptor, yet induced beta

279 known to be critically involved in receptor/G protein coupling, undergoes a major conformational cha

280 The structural determinants of G protein coupling versus activation by G protein-couple

281 es to both receptor stability and functional G-protein coupling via an interaction with the Gbeta sub

282 G protein coupling was examined by quantitative analysis

283 Here the effect of AGS3 on receptor-G protein coupling was examined in an Sf9 cell membrane-

284 G protein coupling was measured by receptor-mediated sti

285 aS binding was reduced, and the reduction in G-protein coupling was accompanied by reduced Ser phosph

286 ly, and the ability of these drugs to induce G-protein coupling was assessed by using GTPgamma(35)S b

287 Agonist-induced receptor-G-protein coupling was of a time scale similar to that o

288 To clarify the role of loop i3 in G protein coupling, we constructed synthetic genes for t

289 nents of the glucagon receptor necessary for G-protein coupling, we replaced sequentially all or part

290 This conclusion was supported by assays of G protein coupling, which documented a loss of agonist-i

291 overexpression of a mutant AT1R incapable of G protein coupling with those of a wild-type receptor.

292 G-protein coupling with CRF(1)-R (forming RG) increased