ライフサイエンスコーパス: G-protein coupling

1 tin coupling, while M153 was dispensable for G protein coupling.

2 is structurally homologous but deficient in G protein coupling.

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

4 tracellular loop also demonstrated broadened G protein coupling.

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

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

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

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

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

10 nsmembrane domains in ligand recognition and G protein coupling.

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

12 protein stability, or allosteric effects on G protein coupling.

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

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

15 ing to arrestin association which interdicts G protein coupling.

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

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

18 the opening of the intracellular crevice for G protein coupling.

19 isplay constitutive activity and promiscuous G protein coupling.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

46 cts the conformational changes necessary for G protein coupling.

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

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

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

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

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

52 in (AM) ligand availability without changing G-protein coupling.

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

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

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

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

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

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

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

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

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

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

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

64 xerting allosteric antagonism and preventing G-protein coupling.

65 outward helical movement of TM6 required for 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 el motifs associated with ligand binding and G-protein-coupling.

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

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

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

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

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

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

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

77 has been demonstrated in mu agonist-induced G protein coupling, adenylyl cyclase activity, receptor

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

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

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

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

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

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

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

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

86 ses of ligands and provide insights into the G protein coupling and selectivity mechanisms adopted by

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

102 easures of efficacy for receptor activation, G protein coupling, and beta-arrestin recruitment for al

103 mon mechanism of class B GPCR activation and G protein coupling, and provide a paradigm for studying

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

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

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

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

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

109 residues involved in receptor activation and G protein coupling are conserved.

110 y discovered as proteins that block receptor-G protein coupling, arrestins are now appreciated for th

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

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

116 minal fragment of C5a, C5a(pep), in terms of G-protein coupling, betaarr recruitment, endocytosis, an

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 lating the agonist structure, biasing toward G-protein coupling but away from long-term down-regulati

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

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

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

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

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

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

129 nderstanding of class F receptor activation, G protein coupling, conformation-based functional select

130 x with heterotrimeric G proteins and whether G-protein coupling contributes to the activation of GLI

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

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

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

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

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

136 3 cells, both the native AT1a receptor and a G protein-coupling deficient DRY/AAY mutant recruited be

137 60 min compared with 76-87% for WT, loss of G protein coupling did not account for differences in in

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

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

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

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

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

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

144 from the extracellular Venus flytraps to the G protein-coupling domains-the 7-transmembrane domains-i

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

176 Several water molecules near the G protein-coupling interface, however, are stable.

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

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

179 e near intracellular loop (ICL) 2/TM3 at the G-protein-coupling interface, suggesting a mechanism of

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

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

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

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

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

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

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

187 ary messenger signaling by directly altering G protein coupling kinetics and efficacy.

188 nist selectivity, and lack of activation and G protein-coupling knowledge have hindered the developme

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

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

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

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

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

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

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

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

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

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

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

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

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

202 G protein coupling of GPR40 was examined in Chinese hams

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

221 vely, our data show that differences in GPCR-G protein coupling preferences, and the Galpha(o) substr

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

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

224 G-protein-coupling profiles govern GPCR-induced cellular

225 /11) and G(12/13) proteins, and complemented G-protein-coupling profiles through a NanoBiT-G-protein

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

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

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

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

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

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

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

233 nserved water-mediated interactions near the G protein-coupling region, along with diverse water-medi

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

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

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

237 The G protein coupling requires the transmembrane domain of

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

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

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

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

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

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

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

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

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

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

248 understanding the molecular determinants of G-protein coupling selectivity.

249 in that is proximal to the N terminus of the G protein-coupling seven-transmembrane-spanning bundle.

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

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

252 lex does not provide a clear explanation for G protein coupling specificity.

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

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

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

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

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

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

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

260 6N, R201A, and R205A also appeared to affect G protein coupling, suggesting that these residues may a

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

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

263 ndertakes an atypical mode of activation and G protein coupling that features a different set of key

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

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

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

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

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

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

270 biochemically characterized agonist-promoted G protein coupling to each CLR.RAMP complex.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

285 oupled receptors (GPCRs), thereby preventing G-protein coupling, triggering receptor internalization

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

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

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

289 G protein coupling was examined by quantitative analysis

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

291 G protein coupling was measured by receptor-mediated sti

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

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

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

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

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

297 ed to chimeric G proteins, EMR2 showed broad G protein-coupling, whereas CD97 coupled more specifical

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

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

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