ライフサイエンスコーパス: protein coupling

1 n intracellular binding site that enhances G-protein coupling.

2 ed the allosteric effect on CRF-stimulated G-protein coupling.

3 processes may be independent of Galpha(q/11) protein coupling.

4 anging ligand binding affinity or receptor-G protein coupling.

5 rting allosteric antagonism and preventing G-protein coupling.

6 acellular loop also demonstrated broadened G protein coupling.

7 s of the G alpha s protein in the receptor/G protein coupling.

8 in GPCR activation and productive receptor/G protein coupling.

9 eatment with GTPgammaS was used to inhibit G protein coupling.

10 s abolished in an AT1 mutant that lacks G(q) protein coupling.

11 ssible role for CaM in regulating receptor-G protein coupling.

12 dependent pathway, which is independent of G protein coupling.

13 membrane domains in ligand recognition and G protein coupling.

14 ity and reduced the efficiency of receptor/G protein coupling.

15 ion profiles, suggestive of selective Galpha protein coupling.

16 tion, (iv) microswitch activation, and (v) G protein coupling.

17 rrestins), which prevents further receptor-G-protein coupling.

18 les in receptor activation and/or receptor/G protein coupling.

19 meric G proteins are required for receptor-G protein coupling.

20 g to arrestin association which interdicts G protein coupling.

21 currents occur at a critical threshold of G protein coupling.

22 tward helical movement of TM6 required for G-protein coupling.

23 hether ERK activation differs according to G-protein coupling.

24 treatment, consistent with S1P receptor/G(i) protein coupling.

25 ed by an increase in intrinsic efficacy of G protein coupling.

26 hat dimerization may be a prerequisite for G protein coupling.

27 of membrane lipid composition on receptor-G protein coupling.

28 nnabinoid receptor 1 (CB1) and antagonized G protein coupling.

29 2+) channels, but lacked voltage-dependent G protein coupling.

30 ain of CXCR4, or pertussis toxin-sensitive G-protein coupling.

31 igher compared with traditional carbodiimide protein coupling.

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

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

34 lass II receptors are the likely sites for G protein coupling.

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

36 r (AT(1)-R) is an important determinant of G protein coupling.

37 gets for modulation of agonist binding and G protein coupling.

38 ould have a significant impact on receptor-G protein coupling.

39 ad distinct kinetic properties in receptor-G protein coupling.

40 tion of G(i) but not required for receptor-G protein coupling.

41 known about quantitative aspects of FPR-G(i) protein coupling.

42 ced agonist potency, binding affinity, and G protein coupling.

43 thosine 5'-triphosphate (XTP)] on receptor/G protein coupling.

44 elationships of each of these residues for G-protein coupling.

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

46 rs, apparently due to promiscuous receptor/G protein coupling.

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

48 on about mechanisms of signal transfer and G protein coupling.

49 ting an inhibitory site distal to receptor/G protein coupling.

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

51 muscarinic receptor as being critical for G-protein coupling.

52 ified where mutations compromised receptor/G-protein coupling.

53 ylcholine receptor for domains that govern G-protein coupling.

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

55 f Ang II may reflect a selective effect on G protein coupling.

56 mediated by changes in receptor density or G protein coupling.

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

58 but is not required for apelin binding or Gi protein coupling.

59 t plays a novel role in regulating 5-HT2AR G protein coupling.

60 PAR1 surface expression and efficiency of G protein coupling.

61 e, an ideal test case for exploring membrane protein coupling.

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

63 s the conformational changes necessary for G protein coupling.

64 n adenylyl cyclase because of differential G-protein coupling.

65 inding to CB1 yet acts as an antagonist of G protein coupling.

66 ike mGluR2, a single 7TM is sufficient for G-protein coupling.

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

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

69 and binding and the efficiency of receptor G-protein coupling.

70 s structurally homologous but deficient in G protein coupling.

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

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

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

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

75 e with SR141716A in antagonizing the basal G protein coupling activity of CB1, as indicated by a redu

76 In contrast basal G protein coupling activity of the three variants was unaf

77 tinct regions critical for ligand binding, G protein coupling activity, and receptor trafficking.

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

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

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

81 rrestin binding, which terminates receptor-G protein coupling, also initiates a second wave of signal

82 ed receptor with intact ligand binding and G-protein coupling and activation, but deficient in recept

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

84 evelop KOR agonists that are biased toward G protein coupling and away from betaarrestin2 recruitment

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

86 r phosphorylation at the level of receptor/G protein coupling and by an unknown mechanism at the leve

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

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

89 iated signaling by increasing both beta2AR-G protein coupling and intrinsic adenylyl cyclase activity

90 h was accompanied by defective D1 receptor G-protein coupling and loss of natriuretic response to SKF

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

92 tein-coupled receptors, thereby preventing G protein coupling and often switching signaling to other

93 geting regions of the receptor involved in G protein coupling and phosphorylation.

94 e receptor signaling by impairing receptor-G-protein coupling and promoting receptor internalization.

95 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 heter

97 R), the activation of KOR promotes Galphai/o protein coupling and the recruitment of beta-arrestins.

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

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

100 T1R occurs independently of heterotrimeric G protein coupling and, if so, the cellular function of su

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

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

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

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

105 inds to the AT(1)R, reduces heterotrimeric G-protein coupling, and inhibits IP(3) (inositol-1,4,5-tri

106 al ligand binding affinity, markedly lower G-protein coupling, and markedly lower chemotaxis toward F

107 uences the ligand-uptake/degradation rate, G protein coupling, and receptor stability.

108 ed similar ligand binding characteristics, G protein coupling, and signal transduction as their respe

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

110 ells expressing AT1 mutants that retain G(q) protein coupling, AngII is still able to induce HB-EGF s

111 we provide new evidence for a specific water-protein coupling as the cause of the observed dynamical

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

113 rmational change that exposes a domain for G protein coupling at the cytosolic surface of the helical

114 nd loop mutant, which lacks heterotrimeric G protein coupling (AT1a-i2m).

115 H3P7) functioned as an actin-binding adaptor protein, coupling BCR signaling and Ag-processing pathwa

116 as G(i) activators rather than in receptor-G protein coupling, because high-affinity agonist binding

117 The G protein coupling behavior of four human 5-hydroxytryptam

118 5-HT1 receptor subtypes exhibit different G protein coupling behaviors.

119 y agonist binding as a measure of receptor-G protein coupling, betagamma-containing gamma11 was the m

120 owed that JF5 was selective with regard to G protein coupling, blocking signaling mediated by G(alpha

121 rtant for the affinity of ligand-dependent G protein coupling but did not affect the maximal signal.

122 nist, the biased ligand (R)-4 induced poor G protein coupling but substantial beta-arrestin recruitme

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

124 ceptors, mGluR1 and mGluR5, occurs through G-protein coupling, but evidence suggests they might also

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

126 ines and opioids tested was able to induce G protein coupling by U51, and no evidence for opioid liga

127 nternalization that is not dependent upon Gi-protein coupling, calcium transients, or protein kinase

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

129 insect cells exhibited ligand binding and G-protein coupling characteristics similar to the wild-typ

130 cking to the cell surface, ligand binding, G protein coupling, chronic desensitization, and down-regu

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

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

133 Co-expression of ligand binding- and G protein coupling-defective mutant receptors did not sign

134 tion from an inherent instability of these G protein coupling-defective receptors.

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

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

137 0 min compared with 76-87% for WT, loss of G protein coupling did not account for differences in inte

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

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

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

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

142 rgic 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 recep

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

145 the transmembrane core to the cytoplasmic G-protein-coupling domains.

146 the mu-opioid receptor regulates receptor-G protein coupling efficacy.

147 tive tissues leads to an enhanced receptor/G protein coupling efficiency that contributes to sensitiz

148 he DRY motif may reduce mu-opioid receptor-G-protein coupling efficiency.

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

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

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

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

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

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

155 e discovered that the specific activity of G protein coupling for single rhos sequestered in individu

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

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

158 he use of more direct measures of receptor-G protein coupling (GTPase activity, GTP gamma S binding),

159 rminants governing the selectivity of GPCR/G protein coupling, however, remain obscure.

160 of spontaneous and ligand-induced receptor-G protein coupling in delta (DOP) and mu (MOP) opioid rece

161 en receptors, we found unique aspects of Vav protein coupling in each receptor pathway.

162 ow almost complete and complete loss of G(i) protein coupling in FPR-F110S and FPR-C126W, respectivel

163 mino acids and may therefore underlie GPCR/G protein coupling in general.

164 xz infusion prevented DAMGO stimulation of G-protein coupling in LPBNi and markedly reduced this stim

165 oint to experience-specific shifts in PAR1-G protein coupling in the amygdala as a novel mechanism re

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

167 These findings implicate abnormal betaAR-G protein coupling in the pathogenesis of the failing hear

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

169 he specific binding of A1-AdoR and A1-AdoR/G protein coupling in ventricular myocardium of 6- to 24-m

170 s and influence the efficiency of receptor-G protein coupling in vitro.

171 utation abolished agonist-induced receptor/G protein coupling in yeast.

172 nositol phosphate production (a measure of G-protein coupling) in association with mutational analysi

173 ortantly, our results indicate a switch in G-protein coupling, in which E775K loses G(o) coupling but

174 everely reduced the efficiency of receptor/G protein coupling, indicating that the targeted residues

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

176 iphosphate binding, which is indicative of G protein coupling inhibition in a concentration-dependent

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

178 binding leads to higher fluctuations in the protein-coupling interface than ARC, especially in the r

179 c coupling of the agonist-binding site and G-protein-coupling interface that may generally be respons

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

181 Thus, lipid-protein coupling is a possible mechanism for both lipid

182 the anterior cingulate cortex: D1 receptor-G protein coupling is greatly reduced, the GABAergic syste

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

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

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

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

187 Because G protein coupling is reported to have a selective effect

188 Pr induces receptor desensitization at the G protein coupling level.

189 tacts from the retinal binding site to the G protein-coupling loops.

190 This suggests that G-protein coupling may be a novel sugar-signaling mechanis

191 ly curved membrane sites through a curvature-protein coupling mechanism that supports the emergence o

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

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

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

195 otential to correct the defective receptor-G protein coupling observed in the high membrane cholester

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

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

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

199 st that fluoxetine gradually increases the G-protein coupling of 5-HT2A/2C receptors without altering

200 he structure of the receptor interface for G protein coupling of a PAFR and suggests a conserved role

201 or their capacity to sterically hinder the G protein coupling of agonist-activated seven-transmembran

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

203 gnificantly affected by the pH of binding, G-protein coupling of CCR5, or partial gp120 deglycosylati

204 G protein coupling of GPR40 was examined in Chinese hamste

205 ylcholine-stimulated increases in receptor-G-protein coupling of M(3)-AChR-N514Y reached only 12% of

206 a conserved role of amphipathic helices in G protein coupling of receptors ranging from those for bio

207 sm and functional consequences of dual Gs/Gi protein coupling of the beta3-adrenergic receptor (beta3

208 PTHrP production are because of alternate G-protein coupling of the receptor in normal versus transf

209 Morphine stimulated G protein coupling of the three receptor variants to a max

210 a-adrenergic receptors, consistent with G(s)-protein coupling of these receptors.

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

212 shed upon treatment with agents that block G-protein coupling or deglycosylate the receptor.

213 ther G protein-coupled receptors, in which G protein coupling or phosphorylation are critical for lon

214 on may modulate the efficiency of receptor-G protein coupling or promote activation of Gbetagamma eff

215 To determine whether functional receptor-G protein coupling or signaling are required for internali

216 ffecting ligand binding affinity, receptor-G protein coupling, or U50,488H-induced desensitization an

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

218 water intake is mediated via the classical G protein coupling pathway, whereas the saline intake caus

219 that the third intracellular loop forms a G-protein coupling pocket comprised of a positively charge

220 ills a structural role forming part of the G-protein coupling pocket, and that A441 contributes to re

221 onformations that are independent of their G protein-coupling potency: one that allows the efficient

222 ology, they show pronounced differences in G-protein coupling preference and the physiological respon

223 perior cervical ganglion (SCG), the mGluR2/G protein coupling profile was characterized by reconstitu

224 (GalRs) have been recently cloned, but the G protein coupling profiles of these receptors are not com

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

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

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

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

229 efficacies were not due to differences in G-protein coupling, receptor desensitization, or recycling

230 the gene encoding the alpha subunit of the G protein-coupling receptors to stimulation of adenylyl cy

231 ion from the chemokine-binding site to the G protein-coupling region we engineered metal ion-binding

232 n this study, we have mutated two putative G protein-coupling regions of CXCR2 and characterized the

233 evidence of any quantitative difference in G protein coupling related to the number of hexadecapeptid

234 e, mechanisms of signal initiation and FZD-G protein coupling remain poorly understood.

235 The G protein coupling requires the transmembrane domain of T1

236 dues on the extracellular side of CXCR4 to G protein-coupling residues on its intracellular side.

237 an normal binding affinity, markedly lower G-protein coupling response, and markedly lower chemotaxis

238 (191) might be responsible for the altered G protein coupling seen with complete enzymatic deglycosyl

239 malian GPCR subfamily displaying different G-protein coupling selectivities.

240 ogy to study mechanisms governing receptor/G protein coupling selectivity and receptor folding.

241 ating that the V2 receptor retained proper G protein coupling selectivity in yeast.

242 of TM VI play key roles in determining the G protein coupling selectivity of the M(3) receptor subtyp

243 The molecular basis of receptor/G protein coupling selectivity was studied by using the m2

244 lgorithm, capable of accurately predicting G-protein coupling selectivity, indicated that both human

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

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

247 residue motions in the ligand-binding and G-protein-coupling sites of the apo receptor are correlate

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

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

250 proach was successful in the prediction of G protein coupling specificity of unknown sequences.

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

252 cytoplasmic tail are determinants of Galpha protein coupling specificity.

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

254 plasmic loop is crucial for determining G(i) protein coupling specificity.

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

256 characterized for functions in addition to G protein coupling, such as receptor phosphorylation and l

257 bited by approximately 50%, despite normal G protein coupling, suggesting a distal inhibitory locus.

258 , R201A, and R205A also appeared to affect G protein coupling, suggesting that these residues may als

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

260 osphorylated active receptors, terminating G protein coupling, targeting receptors to endocytic vesic

261 S107 (a stabilizer of RyR1-FK506 binding protein coupling that reduces Ca(2+) leak) or local expr

262 rotein 95 (PSD-95) is a postsynaptic adaptor protein coupling the NMDA receptor to downstream signall

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

264 ated by Ang II even without heterotrimeric G protein coupling, the carboxyl terminus of the AT1 recep

265 e additive contributions of Ni3 and Ci3 to G-protein coupling, the functional responses of two double

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

267 k complexes bind to and phosphorylate target proteins, coupling their activity to cell cycle states.

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

269 G-protein coupling to 5-HT(1A) receptors and G-protein lev

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

271 Similarly, the degree of G protein coupling to 5-HT1A receptors varied markedly amo

272 te noncanonical ghrelin receptor (GHS-R1a)-G-protein coupling to Galpha(i/o) instead of Galpha(q11) a

273 We were unable to detect Galphaq or Galpha11 protein coupling to homomers or heteromers of D1 or D2 r

274 e previously been shown to be critical for G protein coupling to many other G protein-coupled recepto

275 ns have precluded a definitive analysis of G protein coupling to monomeric GPCRs in a biochemically d

276 In contrast, Gq protein coupling to NTS1 in various lipid nanodiscs was

277 d will allow molecular characterization of G protein coupling to other heptahelical receptors.

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

279 taste receptors or interfere with receptor-G protein coupling to serve as naturally occurring taste m

280 ted that P4pal-10 selectively inhibits all G protein coupling to several Gq-coupled receptors, includ

281 AngII analog that induces betaarr, but not G protein coupling to the AT(1)R, recapitulates the effect

282 onetheless antagonized the agonist-induced G-protein coupling to the CB1 receptor, yet induced beta-a

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

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

285 d receptor conformational dynamics control G protein coupling to trigger signaling is a key but still

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

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

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

289 binding was reduced, and the reduction in G-protein coupling was accompanied by reduced Ser phosphor

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

291 G protein coupling was examined by quantitative analysis o

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

293 G protein coupling was measured by receptor-mediated stimu

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

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

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

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

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

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

300 on proteins constitute a basic mechanism for protein coupling within the replication complex.