ライフサイエンスコーパス: GPCR

1 GPCR dimerization is a well-established phenomenon that

2 GPCR priming suggests another layer of regulation in the

3 GPCR regulation of TRPM3 is also seen in vivo where Gi/o

4 GPCR signalling is negatively regulated by beta-arrestin

5 GPCRs regulate all aspects of human physiology, and biop

6 GPCRs typically recruit arrestins through two different

7 erview of the types of motion exhibited by a GPCR and then discuss GPCR dynamics in the context of li

8 ect the biological processes controlled by a GPCR-independent mechanism of G protein activation media

9 Sensors consist of a GPCR and G protein tethered by an ER/K linker flanked by

10 les can be released across the lifetime of a GPCR.

11 ecent years, the molecular architecture of a GPCR/GRK complex remains poorly defined.

12 Our findings reveal, for the first time, a GPCR as a target for co-regulatory functions of site-spe

13 f related agonists for specific binding to a GPCR.

14 ollowing nerve injury in mice, perhaps via a GPCR-mediated activation mechanism, and suggest that inh

15 ciated with activation mechanisms in class A GPCRs.

16 a template for precision control of Family A GPCRs.

17 of fusion proteins are not consistent across GPCRs.

18 Activated GPCRs undergo clathrin-dependent endocytosis.

19 ibiting impaired dissociation from activated GPCRs) showed that 2PPM is capable of detecting GPCR-G p

20 hich GRKs regulate the function of activated GPCRs.

21 suggest that Gi1 interacts only with active GPCRs and that the well known high speed of GPCR signal

22 ormatics-based study is likely common to all GPCR-activated GRKs.

23 ses signaling potency, suggesting an altered GPCR conformation as the underlying basis for GPCR primi

24 affinity fluorescent probes for 14 aminergic GPCRs.

25 -protein-coupled receptors (termed aminergic GPCRs) belong to the class of cell membrane receptors an

26 y, the prevalence of genetic variation among GPCRs targeted by drugs is unknown.

27 ncreased inositol phosphate accumulation and GPCR-kinase interacting protein-1-GPR75 binding, which f

28 ructural understanding of GPCR/G-protein and GPCR/arrestin complexes has emerged in recent years, the

29 ndeed, guanosine 5'-O-(thiotriphosphate) and GPCR agonists only weakly activate the TRPC5R593A mutant

30 amentally different between GBA proteins and GPCRs, and that GEF-mediated perturbation of nucleotide

31 t require preassembly between G proteins and GPCRs.

32 We discovered that RAMPs and GPCRs tend to have orthologs in the same species and hav

33 to the noncovalent, tightly bound antagonist-GPCR complex of iodopindolol and beta-adrenergic recepto

34 12 kcal/mol more stable than the antagonist-GPCR complex.

35 nate sites on the GPCR, and (iii) asymmetric GPCR dimers.

36 ligand-directed modeling (LDM) to available GPCR X-ray structures to improve VS performance and sele

37 ructural framework for understanding class B GPCR activation through hormone binding.

38 Class B GPCRs are important therapeutic targets; however, our un

39 on of these glycine hinges among all class B GPCRs suggests their general role in activation of these

40 -active Gi1 However, we also show that basal GPCR activity allows interactions between non-stimulated

41 amics control allosteric transitions between GPCR conformations.

42 R-operated Erk1/2 activation differs between GPCRs and the underlying mechanism remains poorly charac

43 nding of functional requirements in biphasic GPCR-betaarr interaction.

44 upied G-protein-coupled receptors (GPCRs) by GPCR kinases (GRKs) functions to turn off G-protein sign

45 oth receptor activity and phosphorylation by GPCR kinases.

46 lation-dependent recruitment of arrestins by GPCRs.

47 that GBAi does not interfere with canonical GPCR-G protein signaling but blocks GBA-dependent signal

48 d sales data, we suggest that characterizing GPCR variants could increase prescription precision, imp

49 though we and others have shown that chronic GPCR stimulation and the consequent upregulated interact

50 s another layer of regulation in the classic GPCR ternary-complex model, with broad implications for

51 ates between Gi/o proteins and their cognate GPCRs in the inactive state (Gi/o-GPCR preassembly).

52 vel Golgi export checkpoint that coordinates GPCR delivery to the surface.

53 by phorbol myristate acetate, Gq/11-coupled GPCR, or epidermal growth factor receptor stimulation pr

54 one is sufficient to abolish the Gi-coupled GPCR-governed TE retraction and subsequent migration of

55 This toolkit of CRISPR-coupled GPCRs provides a modular platform for rewiring diverse l

56 s not clear how the activation of Gi-coupled GPCRs at the LE orchestrates the TE retraction in RAW264

57 Rs) showed that 2PPM is capable of detecting GPCR-G protein interactions.

58 se availability of experimentally determined GPCR/ligand complex structures with diverse ligands impe

59 ay crystal structures across seven different GPCRs bound to a range of ligands of different chemotype

60 motion exhibited by a GPCR and then discuss GPCR dynamics in the context of ligand binding, activati

61 Our results demonstrate that four diverse GPCRs do not preassemble with non-active Gi1 However, we

62 We adopt the design to diverse GPCRs that sense a broad spectrum of ligands, including

63 mechanism, distinct from other multi-domain GPCRs.

64 Endosomal GPCRs are a drug target that deserve further attention.

65 We thus identify Gpr124 as an endothelial GPCR specifically required for endothelial Wnt signaling

66 there are three RAMPs and over 800 expressed GPCRs, making direct experimental approaches challenging

67 rotease-resistant agonists of other B-family GPCRs.

68 xchange has been difficult for all but a few GPCR-G protein complexes.

69 PCR conformation as the underlying basis for GPCR priming.

70 , but not other G-proteins, is essential for GPCR-induced potentiation of Syk phosphorylation downstr

71 ntages, such as an increased selectivity for GPCR subunits and the ability to introduce specific bene

72 in the orthosteric pocket, particularly for GPCRs within a single subfamily, such as the nine adrene

73 minimal ciliary localization sequences from GPCRs and fibrocystin (also implicated in polycystic kid

74 he G-protein betagamma-subunit (Gbetagamma), GPCR-kinase 2, and beta-arrestin are central to various

75 the effect of the membrane matrix on global GPCR self-assembly.

76 On the other hand, GPCR-G protein fusions have been used extensively to und

77 Moreover, it will shed light on how GPCRs selectively couple to and activate their G protein

78 GPCRs for therapeutic intervention, however GPCR X-ray structures are mostly restricted to their ina

79 Imaging GPCR activation in real time in living animals would pro

80 l time by utilizing the clinically important GPCR, sphingosine-1-phosphate receptor 1 (S1P1).

81 erogeneous mutation profiles accumulating in GPCR, PI3K-Akt and FGFR signaling pathways.

82 stic mechanism for the activation process in GPCR, providing insights and structural details that can

83 e insights into the role of this reaction in GPCR signaling.

84 rd with the established role of recycling in GPCR resensitization.

85 However, their role in GPCR-operated Erk1/2 activation differs between GPCRs an

86 nonrandom somatic mutations specifically in GPCR, PI3K-Akt and FGFR signaling pathways.

87 tivated chloride channels such as TMEM16a in GPCR-activation of itch nerve terminals.

88 a unique set of sensory proteins, including GPCRs and other membrane proteins.

89 nctions of cell surface receptors, including GPCRs, remains largely unclear.

90 Here, we present evidence that individual GPCR-G-protein interactions can reinforce each other to

91 eractions of lipid molecules with individual GPCRs, to the effect of the membrane matrix on global GP

92 ell established for detecting ligand induced GPCR-G protein interactions in cells.

93 ng schemes have been combined to investigate GPCR signaling and dynamics at the single-molecule level

94 d that species differences do exist in islet GPCR expression and function, which are likely to impact

95 Our comprehensive human and mouse islet GPCR atlas has demonstrated that species differences do

96 s surrogates for human islets to study islet GPCR function, and we have identified species-specific e

97 e also survey the methodologies for labeling GPCRs with biophysical probes, particularly fluorescent

98 involving the formation of a ternary ligand-GPCR-G-protein complex.

99 ta-arrestins are essential scaffolds linking GPCRs to Erk1/2 signaling.

100 ir relatively accessible cellular locations, GPCRs represent one of the most important classes of the

101 nge of vital physiological processes, making GPCRs prominent drug targets.

102 ight provide new strategies for manipulating GPCR signaling.

103 cific requirement for primary cilia-mediated GPCR signaling in interneuronal connectivity and inhibit

104 derstanding of thermal adaptation in a model GPCR.

105 y, and functionally diverse ligands modulate GPCR function.

106 at protein kinases and phosphatases modulate GPCR signaling, how serine/threonine phosphatases integr

107 of their interaction interfaces to modulate GPCR functions selectively have not been fully explored

108 that Gbeta1 protein enlists PP1c to modulate GPCR signaling in platelets.

109 orms governs the biological effects for most GPCRs, as yet unexplored for the IGF-1R, we sought to in

110 operates through the regulation of multiple GPCRs throughout the hypothalamus.Melanocortin receptor

111 ion of TRPM3 is also seen in vivo where Gi/o GPCRs agonists inhibited and inverse agonists potentiate

112 The observed specificity of Gi/o-GPCR coupling and the high rate of Gi/o signal transduct

113 ir cognate GPCRs in the inactive state (Gi/o-GPCR preassembly).

114 increasing awareness of novel attributes of GPCR function that offer new opportunity for drug develo

115 Herein, we consider how evolving concepts of GPCR pharmacology have shaped understanding of the compl

116 e and investigate functional consequences of GPCR-mediated signaling at the Golgi/trans-Golgi network

117 ese receptors and for the rational design of GPCR-targeted drugs.

118 that enables the bioluminescent detection of GPCR activation in real time by utilizing the clinically

119 ces promise to streamline the development of GPCR-targeted medications.

120 The duration of GPCR-mediated signaling is primarily regulated via GPCR

121 Finally, we discuss the implications of GPCR conformational plasticity for drug design.

122 The majority of GPCR crystal structures published to date were obtained

123 ng (RGS) proteins are critical modulators of GPCR activity, yet their role in beta cells remains larg

124 discovery efforts, and there are a number of GPCR drugs that have been discovered by use of structura

125 ly inert ground state is an integral part of GPCR signaling.

126 extensively to understand the selectivity of GPCR signaling pathways.

127 GPCRs and that the well known high speed of GPCR signal transduction does not require preassembly be

128 have a major impact on our understanding of GPCR biology.

129 l studies have deepened our understanding of GPCR conformational regulation by different ligands.

130 While a structural understanding of GPCR/G-protein and GPCR/arrestin complexes has emerged i

131 nucleotide exchange factor (GEF) activity of GPCRs.

132 chitecture and to investigate the binding of GPCRs and other receptors to the BBSome.

133 Our results suggest global coevolution of GPCRs and RAMPS and support the hypothesis that GPCRs in

134 Determining the structural dynamics of GPCRs is thus essential both for understanding the physi

135 tor 1 (PTHR1) is a member of the B-family of GPCRs; these receptors are activated by long polypeptide

136 Considering the evolutionary history of GPCRs allows the identification of these selectivity-det

137 eroid influences the spatial organization of GPCRs within the membrane bilayer, and consequently can

138 al variation in enhancing the performance of GPCRs in response to cold temperatures.

139 onist ligands are required for a plethora of GPCRs for therapeutic intervention, however GPCR X-ray s

140 selectivity in extracellular recognition of GPCRs by monoclonal antibodies.

141 tanding of the pharmacological regulation of GPCRs now extends beyond simple competitive agonism or a

142 dings reveal a common structural scaffold of GPCRs that is important for receptor folding and activat

143 gonist-induced endocytosis of a broad set of GPCRs without affecting ERK MAP kinase activation.

144 receptors is a recently deorphanized set of GPCRs, the members of which are now receiving substantia

145 AMP1 and RAMP3 interact with the same set of GPCRs, which implies functional redundancy.

146 ochemical integrator of three major types of GPCRs and necessitate reconsideration of classic models

147 A was found to be a ligand for a variety of GPCRs with a propensity for potent binding across therap

148 herapeutic monoclonal antibodies that act on GPCRs.

149 w the progress in single-molecule studies on GPCRs.

150 restin system as a key regulator of not only GPCRs, but also receptor tyrosine kinases, including the

151 and cancer evolution, particularly in OR1B1 (GPCR signaling pathway) for adenoma evolution, and LAMA1

152 monstrating a potential role for this orphan GPCR in regulating the proliferative capacity of the int

153 Orphan GPCRs provide an opportunity to identify potential pharm

154 unds, especially for understudied and orphan GPCRs.

155 Other GPCRs, however, neither bind covalently to ligands nor a

156 pendent Erk1/2 stimulation elicited by other GPCRs such as beta2-adrenergic, FSH and CXCR4 receptors,

157 We show that the activation of other GPCRs, such as the ADP receptors and protease-activated

158 contexts in vivo and can be applied to other GPCRs.

159 e is evidence APJ heterodimerizes with other GPCRs; however, the existence of APJ homodimers and olig

160 tested whether activation of one particular GPCR, a metabotropic glutamate receptor (mGluR), can red

161 upling to every known major binding partner [GPCRs, Gbetagamma, effectors, guanine nucleotide dissoci

162 betagamma liberated from other photoreceptor GPCRs is also likely to regulate synaptic transmission.S

163 beta2-adrenoceptor (beta2AR), a prototypical GPCR, and then investigate the effects of Vps34 inhibiti

164 X-ray crystallography provided GPCR molecular architectures, which also revealed the ne

165 In addition, the resulting RAMP-GPCR interaction map suggests that RAMP1 and RAMP3 inter

166 However, whether RAMP-GPCR interactions are widespread, and the nature of thei

167 ion triggered by G protein-coupled receptor (GPCR) activation underlies many fundamental physiologica

168 vation following G-protein coupled receptor (GPCR) activation.

169 r (beta1AR) is a G protein-coupled receptor (GPCR) and the predominant adrenergic receptor subtype in

170 The endothelial G-protein-coupled receptor (GPCR) Gpr124 has been reported to be required for normal

171 The G protein-coupled receptor (GPCR) MRGPRD is selectively expressed by a subset of mou

172 ling through the G protein coupled receptor (GPCR) S1pr2, plays a key role in pancreas development li

173 G protein-coupled receptor (GPCR) signaling occurs in complex spatiotemporal pattern

174 The G protein-coupled receptor (GPCR) signaling pathways mediating information exchange

175 s a prototypical G protein-coupled receptor (GPCR) signaling system, in which light-activated rhodops

176 scape determines G-protein-coupled receptor (GPCR) signalling via intracellular binding partners (IBP

177 in the field of G protein-coupled receptor (GPCR) structural biology.

178 R15 is an orphan G protein-coupled receptor (GPCR) that serves for an HIV coreceptor and was also rec

179 ownstream of the G-protein-coupled receptor (GPCR)-Gq/11-phospholipase C (PLC) pathway.

180 involvement of a G protein-coupled receptor (GPCR).

181 LP-1 receptor, a G-protein coupled receptor (GPCR).

182 ious aspects of G protein-coupled receptors (GPCR) expression and signalling.

183 s engagement of G protein-coupled receptors (GPCR) on platelets that promote their aggregation.

184 stimulation of G protein-coupled receptors (GPCR).

185 bind to several G-protein-coupled receptors (GPCRs) activating a number of different signaling networ

186 ass B family of G-protein-coupled receptors (GPCRs) and have opposing physiological roles in insulin

187 family A of the G protein-coupled receptors (GPCRs) and is a potential pharmacotherapeutic target for

188 hodopsin family G protein-coupled receptors (GPCRs) and the polycystic kidney disease-causing polycys

189 G protein-coupled receptors (GPCRs) are central to many fundamental cellular signalin

190 G protein-coupled receptors (GPCRs) are considered to function primarily at the plasm

191 G protein-coupled receptors (GPCRs) are essential for transferring extracellular sign

192 l equilibria of G-protein-coupled receptors (GPCRs) are intimately involved in intracellular signalin

193 ough individual G-protein-coupled receptors (GPCRs) are known to activate one or more G proteins, the

194 G-protein-coupled receptors (GPCRs) are the largest and most diverse group of membran

195 Although 108 G-protein-coupled receptors (GPCRs) are the targets of 475 ( approximately 34%) Food

196 e importance of G protein-coupled receptors (GPCRs) as pharmaceutical targets, there has been an imme

197 transduction of G protein-coupled receptors (GPCRs) at the plasma membrane.

198 gonist-occupied G-protein-coupled receptors (GPCRs) by GPCR kinases (GRKs) functions to turn off G-pr

199 Family A G protein-coupled receptors (GPCRs) control diverse biological processes and are of g

200 G protein-coupled receptors (GPCRs) exhibit highly conserved activation and signaling

201 Resetting of G-protein-coupled receptors (GPCRs) from their active state back to their biologicall

202 , the 826 human G protein-coupled receptors (GPCRs) govern a wide range of vital physiological proces

203 trafficking by G protein-coupled receptors (GPCRs) has focused mainly on endocytic trafficking.

204 G protein-coupled receptors (GPCRs) have evolved a seven-transmembrane helix framewor

205 bers of class B G protein-coupled receptors (GPCRs) in mammalian cells with the incorporation efficie

206 While several G-protein coupled receptors (GPCRs) influence synaptic transmission at ribbon synapse

207 superfamily of G protein-coupled receptors (GPCRs) mediates a wide range of physiological responses

208 re agonists for G-protein-coupled receptors (GPCRs) on platelets.

209 G protein-coupled receptors (GPCRs) play an important role in drug therapy and repres

210 G-protein-coupled receptors (GPCRs) play critical roles in regulating brain function.

211 G-protein-coupled receptors (GPCRs) play critical roles in regulating physiological p

212 G protein-coupled receptors (GPCRs) play crucial roles in cell physiology and pathoph

213 G-protein-coupled receptors (GPCRs) pose challenges for drug discovery efforts becaus

214 G protein-coupled receptors (GPCRs) regulate many animal behaviors.

215 Class B G protein-coupled receptors (GPCRs) respond to paracrine or endocrine peptide hormone

216 are a family of G-protein-coupled receptors (GPCRs) that are irreversibly activated by proteolytic cl

217 Pairing orphan G protein-coupled receptors (GPCRs) with their cognate endogenous ligands is expected

218 G protein-coupled receptors (GPCRs), a superfamily of cell-surface receptors involved

219 and especially G protein-coupled receptors (GPCRs), as next-generation targets.

220 ernalization of G protein-coupled receptors (GPCRs), beta-arrestins are essential scaffolds linking G

221 stimulation of G protein-coupled receptors (GPCRs), including adrenergic and endothelin (ET) recepto

222 to nonolfactory G protein-coupled receptors (GPCRs), including those associated with the central nerv

223 carried out by G-protein-coupled receptors (GPCRs), non-receptor guanine-nucleotide exchange factors

224 G protein-coupled receptors (GPCRs), the largest family of signaling receptors, are c

225 ke most class B G protein-coupled receptors (GPCRs), there is limited knowledge linking biological ac

226 are inhibitory G protein-coupled receptors (GPCRs), to decrease the excitability of dopamine neurons

227 G protein-coupled receptors (GPCRs), which are modulated by a variety of endogenous a

228 The function of G protein-coupled receptors (GPCRs)-which represent the largest class of both human m

229 t interact with G-protein-coupled receptors (GPCRs).

230 of which act on G protein-coupled receptors (GPCRs).

231 eukaryotes, the G protein-coupled receptors (GPCRs).

232 be activated by G protein-coupled receptors (GPCRs).

233 g to class A of G-protein-coupled receptors (GPCRs).

234 l mechanism via G protein-coupled receptors (GPCRs).

235 e activation of G-protein-coupled receptors (GPCRs).

236 l complexity of G protein-coupled receptors (GPCRs).

237 iverse group of G protein-coupled receptors (GPCRs).

238 specificity of G-protein-coupled receptors (GPCRs).

239 have implicated G protein-coupled-receptors (GPCRs) in cancer progression and the acquisition of TIC

240 he only strategy to develop drugs regulating GPCR activity was through the identification of compound

241 her elucidate the role of GRKs in regulating GPCR-mediated behaviors, we utilized the genetic model s

242 ondary to CHF associated with elevated renal GPCR-Gbetagamma signaling and ET system expression.

243 igated the possible salutary effect of renal GPCR-Gbetagamma inhibition in CKD developed in a clinica

244 ealing an unexpected specificity of selected GPCR intracellular signalling components.

245 ough one or more of these metabolite-sensing GPCRs likely contributes to human diseases such as asthm

246 We found several GPCRs that are only expressed in the PGE2-G responder ce

247 ified species-specific expression of several GPCRs.

248 y allows interactions between non-stimulated GPCRs and Gi1 (basal coupling).

249 tween the Gi1 protein and the non-stimulated GPCRs.

250 ations that can be instrumental for studying GPCRs.

251 epresent the best-understood example of such GPCR signaling.

252 The present data support GPCR signaling based on dynamic interactions between two

253 nd how surface delivery of newly synthesized GPCRs is regulated by extracellular signals is less unde

254 etaD2 release from wild-type, but not Takeda GPCR 5(-/-), mice.

255 Effects of DCA were mimicked by the Takeda GPCR 5 agonist, INT-777 (50 muM), but not by the farneso

256 ly, therapeutic drugs are designed to target GPCRs at the plasma membrane.

257 ts have traditionally been pursued to target GPCRs, allosteric modulators provide several mechanistic

258 eam second messengers, a phenomenon we term "GPCR priming." Specifically, we find that the presence o

259 Using this technique, termed "GPCR-APEX," we track activation and internalization of t

260 Based on these findings, we propose that GPCR signaling from endosomes functions as a biologic no

261 nergic receptor (alpha1-AR), suggesting that GPCR priming is a receptor-specific phenomenon.

262 g data from 68,496 individuals, we find that GPCRs targeted by drugs show genetic variation within fu

263 Rs and RAMPS and support the hypothesis that GPCRs interact globally with RAMPs in cellular signaling

264 ical and biophysical studies have shown that GPCRs exist temporally in an ensemble of interchanging c

265 We have systematically compared the GPCR mRNA expression in human and mouse islets to determ

266 hich light-activated rhodopsin (Rho*) is the GPCR catalyzing the exchange of GDP for GTP on the heter

267 tudies carried out on various members of the GPCR family, including rhodopsin (visual receptor), opio

268 Here conformational substates of the GPCR rhodopsin are investigated in micelles of dodecyl m

269 onstrated that selective inactivation of the GPCR-associated protein beta-arrestin 2 in hepatocytes o

270 hway have yielded several antagonists of the GPCR-like smoothened receptor.

271 distinct allosteric and cognate sites on the GPCR, and (iii) asymmetric GPCR dimers.

272 ty of the full agonist-bound form primes the GPCR to couple to IBPs.

273 nown to activate one or more G proteins, the GPCR-G-protein interaction is viewed as a bimolecular ev

274 In Hedgehog (Hh) signaling, the GPCR-family protein Smoothened (Smo) acts as a signal tr

275 ion of Galphas or Galphaq C termini with the GPCR increases signaling potency, suggesting an altered

276 functional assays were performed with these GPCR mutants, including ligand binding, ligand-induced r

277 Ciliary enrichment of these GPCRs thus operates via distinct mechanisms in different

278 determines trafficking of a subset of these GPCRs to neuronal cilia.

279 iding a comprehensive assessment of how this GPCR binds and signals.

280 Thus, GPCRs function not only at the plasma membrane but also

281 Our approach to GPCR NMR creates a framework for exploring how different

282 ark comparing LDM-refined binding pockets to GPCR X-ray crystal structures across seven different GPC

283 lar mechanisms regulating the sensitivity to GPCR-Gq/11-PLC-dependent gating of a receptor-operated c

284 s critical for conferring the sensitivity to GPCR-Gq/11-PLC-dependent gating on TRPC5.

285 f Gd(3+) rescues the mutant's sensitivity to GPCR-Gq/11-PLC-dependent gating.

286 Computational studies on ligand binding to GPCRs have revealed transient, low-affinity binding site

287 xameric complex was identified that binds to GPCRs with interactions that only partially overlap with

288 ternative architectures for fusing CRISPR to GPCRs utilizing the previously reported design, Tango, a

289 opportunities to accelerate progress towards GPCR-targeted flukicides for Fasciola hepatica.

290 Current methods for tracking GPCR signaling suffer from low throughput, modification

291 vided the first evidence that APP fine tunes GPCR signaling and trafficking.

292 nd provide a novel framework for fine-tuning GPCR functions with potential therapeutic implications.

293 deficit, we generated samples of a wild-type GPCR (A2AR) that are deuterated apart from (1)H/(13)C NM

294 n transmitting the signal employing a unique GPCR activation mechanism, distinct from other multi-dom

295 ediated signaling is primarily regulated via GPCR kinase (GRK)-mediated phosphorylation of activated

296 ural and synthetic extracellular signals via GPCRs.

297 c fusion toxin protein that binds this viral GPCR.

298 Whether GPCRs in endosomes control pathophysiological processes

299 nd the lipids that they encode interact with GPCRs that regulate gastrointestinal tract physiology.

300 kinases, GRKs rely on their interaction with GPCRs for activation and not phosphorylation.