ライフサイエンスコーパス: arrestin

1 pine on endogenous M3R is biased toward beta-arrestin.

2 and a displaced C-tail, hallmarks of active arrestin.

3 ta sheet with the N-terminal beta strands of arrestin.

4 showed reduced relative efficacy toward beta-arrestin.

5 nd are then inactivated by a GPCR kinase and arrestin.

6 its phosphorylated C-terminal tail with beta-arrestin.

7 xis or G protein signaling, but they recruit arrestin.

8 r binding partners (IBPs), e.g., Gs and beta-arrestin.

9 Mutant Q301E(7.39) did not recruit arrestin.

10 ptor-transducer interactions with Gs, Gi and arrestin.

11 ugh the multifunctional adapter protein beta-arrestin.

12 ns the structural rearrangements within beta-arrestins.

13 rimeric G proteins, GPCR kinases (GRKs), and arrestins.

14 which engender distinct functionality of ss-arrestins.

15 ascades are controlled by G proteins or beta-arrestins.

16 ut nonexclusively, either G-proteins or beta-arrestins.

17 or kinases and subsequently bound by cognate arrestins.

18 nd activation process between GPCRs and beta-arrestins.

19 and could be elicited by G proteins or beta-arrestins.

20 d receptor that couples to Gi/o proteins and arrestins.

21 cytoplasmic loops, and subsequent binding of arrestins.

22 loop (V2R(DeltaICL3)) can interact with beta-arrestin 1 (betaarr1) only through the phosphorylated ta

23 ic G proteins and the scaffold proteins beta-arrestin 1 and 2.

24 e that ERK1/2 activation is mediated by beta-arrestin 1 from receptors localized exclusively at Rab4/

25 Adult mice lacking beta-arrestin 1 selectively in hepatocytes did not show any c

26 l peptide competed for association with beta-arrestin 1, and phosphorylated central or distal C-termi

27 Our data reveal beta-arrestin 1, beta-arrestin 2, and AT1R as key regulatory

28 ndent myofilament Ca(2+) sensitivity in beta-arrestin 1, beta-arrestin 2, and AT1R knockout mice.

29 emodynamics, we found that mice lacking beta-arrestin 1, beta-arrestin 2, or AT1R were unable to gene

30 er complex as a gatekeeper, terminating beta-arrestin 1-mediated ERK phosphorylation.

31 G proteins and the scaffolding proteins beta-arrestin 1/2.

32 eptide to block the interaction between beta-arrestin-1 and PLCgamma abolishes TRV120027-induced TRPC

33 phospholipase C (PLCgamma) to the AT1R-beta-arrestin-1 signalling complex.

34 Within this paradigm, M3D-arr recruited beta-arrestin-1 to the plasma membrane, and promoted phosphoi

35 Replacing the C-terminal region of beta-arrestin-1 with its counterpart on beta-arrestin-2 or us

36 Here we reveal that TRV120027, a beta-arrestin-1-biased agonist of the angiotensin II receptor

37 orylated vasopressin-2 receptor tail to beta-arrestin-1.

38 t strategies aimed at enhancing hepatic beta-arrestin 2 activity could prove useful for suppressing H

39 which steer the ligand bias between the beta-arrestin 2 and G protein pathway.

40 We identified beta-arrestin 2 as the target gene of miR-365 by bioinformati

41 firmed with a NanoLuc Binary Technology beta-arrestin 2 assay, imaging of green fluorescent protein-t

42 -tagged beta-arrestin 2, and PathHunter beta-arrestin 2 assay.

43 reased the activation of G proteins and beta-arrestin 2 by J113863.

44 However, hepatocyte-specific beta-arrestin 2 deficiency did not affect hepatic insulin sen

45 , hepatocyte-specific overexpression of beta-arrestin 2 greatly reduced hepatic GCGR signaling and pr

46 tivation of the GPCR-associated protein beta-arrestin 2 in hepatocytes of adult mice results in great

47 exon 7-associated C-terminal tails with beta-arrestin 2 in morphine-induced desensitization and toler

48 orphine tolerance through regulation of beta-arrestin 2 in rats.

49 estin 3 with unaltered behavioral effects in arrestin 2 KOs.

50 d the bias of several mu opioids toward beta-arrestin 2 over G protein activation compared with the e

51 ads to receptor internalization and the beta-arrestin 2 recruitment with potency comparable to that o

52 h in G protein-mediated pathways and in beta-arrestin 2 recruitment, no ligand-independent activity c

53 However, we observed a recruitment of beta-arrestin 2 to a GPR27V2 chimera in the presence of membr

54 Our data reveal beta-arrestin 1, beta-arrestin 2, and AT1R as key regulatory molecules in the

55 Ca(2+) sensitivity in beta-arrestin 1, beta-arrestin 2, and AT1R knockout mice.

56 ing of green fluorescent protein-tagged beta-arrestin 2, and PathHunter beta-arrestin 2 assay.

57 over that excessive Krz, the Drosophila beta-arrestin 2, inhibits Smo sumoylation and prevents Smo ac

58 ound that mice lacking beta-arrestin 1, beta-arrestin 2, or AT1R were unable to generate a Frank-Star

59 or CCR5 also induced the recruitment of beta-arrestin 2, whereas UCB35625 did not.

60 Long-term beta-arrestin 2-biased agonism of the angiotensin II receptor

61 ) for 3 months with either TRV120067, a beta-arrestin 2-biased ligand of the angiotensin II receptor,

62 ciliary localization in neurons lacking beta-arrestin 2.

63 peptides competed for association with beta-arrestin 2.

64 um responses were profoundly reduced in beta-arrestin-2 (barr2) deficient beta-cells.

65 Knockout of beta-arrestin-2 (betaarr-2(-/-)) attenuates the asthma phenot

66 led receptor kinase 5, thereby inducing beta-arrestin-2 biased PAR1 signaling by both APC and thrombi

67 ombin exerts cytoprotective effects via beta-arrestin-2 biased PAR1 signaling.

68 ein, Gs, is greater in females, whereas beta-arrestin-2 coupling is greater in males.

69 Here we show that inactivation of the beta-arrestin-2 gene, barr2, in beta-cells of adult mice grea

70 The PAR1-dependent recruitment of beta-arrestin-2 in response to LPS by both APC and thrombin w

71 beta-arrestin-1 with its counterpart on beta-arrestin-2 or using a specific TAT-P1 peptide to block t

72 A homologous arrestin-2 peptide, which differs only in four positions

73 ntly represent biased agonists favoring beta-arrestin-2 recruitment over canonical G protein activati

74 ligand adrenaline in cAMP accumulation, beta-arrestin-2 recruitment, and receptor internalization ass

75 tional selectivity for muOR and minimal beta-arrestin-2 recruitment.

76 h Gs-dependent signaling in females and beta-arrestin-2 signaling in males.

77 inds to APJ, activates the Galphai1 and beta-arrestin-2 signaling pathways, and induces receptor inte

78 C26 recruited beta-arrestin-2, and internalized the Green Fluorescent Prote

79 ve state, leading to the recruitment of beta-arrestin-2.

80 M390 and JNJ20788560) preferentially recruit arrestin 3 and, surprisingly, KO of arrestin 3 produces

81 This study reveals a novel role for arrestin 3 as a facilitator of receptor resensitization.

82 ted by agonist stimulation and competes with arrestin 3 binding to the receptor.

83 in plasma membrane recruitment of endogenous arrestin 3 following alpha2AAR activation.

84 Arrestin 3 is in pre-engaged complexes with the delta op

85 Surprisingly, arrestin 3 KO revealed an acute tolerance to these low-i

86 The disruption of these complexes in arrestin 3 KOs likely accounts for the altered responses

87 recruit arrestin 3 and, surprisingly, KO of arrestin 3 produces acute tolerance and impaired recepto

88 alization and had a less extensive effect on arrestin 3 recruitment but significantly uncoupled the r

89 endocytosis and signaling through disrupting arrestin 3 recruitment.

90 RM390, JNJ20788560) preferentially recruited arrestin 3 with unaltered behavioral effects in arrestin

91 ndreds of diverse receptors and also promote arrestin-3 activation by IP6.

92 osphate (IP6) is a non-receptor activator of arrestin-3 and report the structure of IP6-activated arr

93 -3 and report the structure of IP6-activated arrestin-3 at 2.4-A resolution.

94 IP6-activated arrestin-3 exhibits an inter-domain twist and a displace

95 A unique aspect of arrestin-3 is its ability to support both receptor-depen

96 The arrestin-3 peptide is the smallest MAPK scaffold known.

97 energy transfer assays for Gi activation and arrestin-3 recruitment in human embryonic kidney 293 cel

98 betaAR signaling preferentially through beta-arrestin, a concept known as beta-arrestin-biased agonis

99 sample was found to contain antibodies to S-arrestin, a retinal protein and potent cause of autoimmu

100 inase 1/2 signaling while failing to recruit arrestin, activate inositol phosphate signaling, or inte

101 on phenomenon among GPCRs, this mode of beta-arrestin activation may represent a novel mechanism of s

102 R signalling is negatively regulated by beta-arrestins, adaptor molecules that also activate differen

103 of the PAR4-P2Y12 heterodimer promotes beta-arrestin and Akt co-localization to intracellular vesicl

104 o involve scaffolding proteins, such as beta-arrestin and clathrin.

105 ide new insights into the activation of beta-arrestins and reveal their novel role in receptor cross-

106 -scavenging receptor, does not activate beta-arrestins, and is widely expressed by many leukocyte sub

107 terminus, which was responsible for the beta-arrestin- and GPCR kinase-dependent endocytosis of GPR15

108 ubunit (Gbetagamma), GPCR-kinase 2, and beta-arrestin are central to various cardiovascular diseases,

109 In this study, we investigated whether beta-arrestins are able to bind second messenger kinase-phosp

110 beta-arrestins are critical signalling molecules that regulat

111 of G protein-coupled receptors (GPCRs), beta-arrestins are essential scaffolds linking GPCRs to Erk1/

112 beta-Arrestins are key regulators and signal transducers of G

113 concentrations of either G-proteins or beta-arrestins, as well as by phosphorylation or interactions

114 In beta-arrestin assays, SARs were different, indicating biased

115 valuated at the human GPR84 in cAMP and beta-arrestin assays.

116 nly G(i/o)- but they can also influence beta-arrestin- (betaArr)-mediated signaling.

117 Beta-arrestins (betaarrs) critically mediate desensitization,

118 understand the relative contribution of beta-arrestin bias to the efficacy of select beta-blockers, a

119 ligand screened, nor is it required for beta-arrestin-bias activated by the beta2AR subtype of the be

120 gnaling and suggest that the concept of beta-arrestin-bias may need to be refined to incorporate the

121 rough beta-arrestin, a concept known as beta-arrestin-biased agonism.

122 beta-blocker, has been classified as a beta-arrestin-biased agonist that can inhibit basal signaling

123 ta2AR expression is unaltered in CHF, a beta-arrestin-biased agonist that operates through the beta2A

124 ly can be targeted therapeutically with beta-arrestin-biased AT1R ligands.

125 ta2ARKO BM with rescued expression of a beta-arrestin-biased beta2AR in vivo restored BM CCR2 express

126 We show that endomorphin-2 (EM2), an arrestin-biased ligand for microR, lengthens surface lif

127 In the present study, by expressing an arrestin-biased M3 muscarinic receptor-based DREADD (M3D

128 acy of select beta-blockers, a specific beta-arrestin-biased pepducin for the beta2AR, intracellular

129 thened endocytic lifetimes were required for arrestin-biased signaling by EM2.

130 lar loop (ICL)1-9, was used to decouple beta-arrestin-biased signaling from occupation of the orthost

131 In contrast, cannabinoids that are beta-arrestin-biased--such as THC found at high levels in mod

132 ed within the context of the photochemistry, arrestin binding and turnover of the visual pigments loc

133 pothesis, a shifting balance between the two arrestin binding modes determines the degree of ERK acti

134 High-affinity arrestin binding requires receptor phosphorylation, ofte

135 nts in living cells are consistent with beta-arrestin binding to M1 muscarinic acetylcholine receptor

136 s suggests a competition for CRIP1a and beta-arrestin binding to the CB1R, which we hypothesized coul

137 It develops within seconds of arrestin binding to the M1 receptor, and it reverses wit

138 phosphorylate activated receptors to promote arrestin binding, decoupling from heterotrimeric G prote

139 ates in complexes with either CRIP1a or beta-arrestin, but CRIP1a and beta-arrestin fail to coimmunop

140 emonstrate that Ang II receptors engage beta-arrestin, but not Gq, to mediate ARF6 activation in HEK

141 for phosphorylation-dependent recruitment of arrestins by GPCRs.

142 s that lifetimes of agonist-induced receptor-arrestin clusters at the cell surface control the magnit

143 roR, lengthens surface lifetimes of receptor-arrestin clusters significantly compared with morphine.

144 tep for Erk recruitment to the receptor/beta-arrestin complex and Erk activation.

145 volved in the stabilization of the GHSR1a-ss-arrestin complex in a manner that determines the ultimat

146 ken together, our results show that the GPCR-arrestin complex initiates non-desensitized signalling a

147 er (XFEL) crystal structure of the rhodopsin-arrestin complex, in which the phosphorylated C terminus

148 ral understanding of GPCR/G-protein and GPCR/arrestin complexes has emerged in recent years, the mole

149 on of beta-arrestin with GPCRs, and the beta-arrestin conformational changes in real time and in livi

150 similarly depend on both G-protein and beta-arrestin D2R signaling.

151 by which the PAR4-P2Y12 dimer controls beta-arrestin-dependent Akt signaling is not known.

152 ression, which itself was regulated via beta-arrestin-dependent beta2AR signaling.

153 rmore, beta-blocker carvedilol-mediated beta-arrestin-dependent ERK activation is significantly reduc

154 2 phosphorylation at Thr(383) underlies beta-arrestin-dependent Erk1/2 activation by GPCRs.

155 Thr(383) phosphorylation is involved in beta-arrestin-dependent Erk1/2 stimulation elicited by other

156 e) is generally believed to be necessary for arrestin-dependent functional outcomes such as receptor

157 ed questions that limit understanding of how arrestin-dependent GPCR signaling controls cell function

158 antagonist with regard to G protein and beta-arrestin-dependent intracellular signaling.

159 tors, which engage Erk1/2 pathway via a beta-arrestin-dependent mechanism, promotes MEK-dependent bet

160 3 (GRK3) nor cell-specific deletion of GRK3/arrestin-dependent p38alpha MAPK from dopamine neurons b

161 ELA activated G-protein- and beta-arrestin-dependent pathways.

162 ceptors, signals through G-protein- and beta-arrestin-dependent pathways.

163 ternalization and desensitization, which are arrestin-dependent processes.

164 verse to G-protein-dependent signaling, beta-arrestin-dependent signaling promotes cardiomyocyte surv

165 hat these disruptive effects did not require arrestin-dependent signaling, because neither global del

166 se 1/2 (ERK1/2) was G protein-, but not beta-arrestin-, dependent.

167 ARMMs (arrestin domain-containing protein 1 (ARRDC1)-mediated m

168 he induction of the glucose-responsive genes arrestin domain-containing protein 4 (ARRDC4) and thiore

169 the mechanisms and cascades mediated by beta-arrestins downstream from the CB1R.

170 pathway but are weaker agonists for the beta-arrestin engagement and subsequent endocytosis toward th

171 Ligand-specific recruitment of arrestins facilitates functional selectivity of G-protei

172 CRIP1a or beta-arrestin, but CRIP1a and beta-arrestin fail to coimmunoprecipitate with each other.

173 he Rsp5 ubiquitin-ligase, recruited by alpha-arrestin-family adaptors.

174 We show that by collaborating with beta-arrestin, Flna maintains the homeostatic signaling betwe

175 u-opioid receptor, which do not recruit beta-arrestin following receptor activation.

176 Thus, CRIP1a can compete with beta-arrestins for interaction with C-terminal CB1R domains t

177 the sustained binding between GPCRs and beta-arrestins, formed by phosphorylated serine-threonine clu

178 ntly, we show that effector-binding sites on arrestins have distinct conformations in the basal and a

179 ons with three positively charged pockets in arrestin in a mode that resembles binding of the phospho

180 ilar intramolecular conformational change in arrestin in either binding mode.

181 in dependent and partially dependent on beta-arrestin in HEK293 cells, and nearly half of the interna

182 to DISC1, and upregulation of DISC1 and beta-Arrestin in hippocampus and amygdala.

183 single amino acid substitutions in ACKR3 on arrestin in response to CXCL12 or CXCL11.

184 enting the recruitment of G proteins or beta-arrestins, in agreement with the lack of signalling resp

185 XCR4 receptors, but does not affect the beta-arrestin-independent Erk1/2 activation by 5-HT4 receptor

186 ons disrupts behavioral inhibition in a GRK3/arrestin-independent manner and suggests that KOR antago

187 pioid antidepressants by an uncharacterized, arrestin-independent mechanism.

188 tion pathways studied: cAMP production, beta-arrestin interaction, and MAP kinase activity.

189 y lock not only stabilizes the receptor-beta-arrestin interaction, but also governs the structural re

190 if that regulates calcium signaling and beta-arrestin interactions.

191 The interaction between receptors and beta-arrestins is generally believed to require both receptor

192 ts from controlled expression of either beta-arrestin isoform demonstrate that beta-arrestin2 acts in

193 ilities of IGF-1R to interact with each beta-arrestin isoform, depending on the presence of the ligan

194 lar 3D structures, the widely expressed beta-arrestin isoforms 1 and 2 play at times identical, disti

195 Because the interplay between beta-arrestin isoforms governs the biological effects for mos

196 nstrates the antagonism between the two beta-arrestin isoforms in controlling IGF-1R expression and f

197 ling, insensitive to pertussis toxin or beta-arrestin knock-out, and mimicked by Gs-DREADD stimulatio

198 previously unrecognized interaction of beta-arrestin localized to the sarcomere.

199 purinergic receptor P2Y12 to coordinate beta-arrestin-mediated Akt signaling, an important mediator o

200 tion of specific G-protein dependent or beta-arrestin-mediated cascade pathways.

201 the plasma membrane, followed by rapid beta-arrestin-mediated desensitization and receptor internali

202 mains that could affect agonist-driven, beta-arrestin-mediated internalization of the CB1R.

203 ria by regulating Duox expression through an Arrestin-mediated MAPK JNK/ERK phosphorylation cascade.

204 pathways, e.g., the Galphai-mediated and the arrestin-mediated pathways for microR.

205 CXCL12 and signals exclusively through beta-arrestin-mediated pathways, without activating canonical

206 is dependent on Galphaq/11-mediated or beta-arrestin-mediated signaling but rather involves liberati

207 owing endocytosis was sufficient to increase arrestin-mediated signaling by both EM2 and the clinical

208 cines to alanines decreased the magnitude of arrestin-mediated signaling by EM2 without affecting G-p

209 nstitute a comprehensive description of beta-arrestin-mediated signaling from CB1Rs and suggest modul

210 identify the retromer as a modulator of beta-arrestin-mediated signaling from CB2R.

211 Here we provide a comprehensive view of beta-arrestin-mediated signaling from the cannabinoid 1 recep

212 tor endocytic lifetimes and the magnitude of arrestin-mediated signaling, and implicate these sequenc

213 to turn off G-protein signaling and turn on arrestin-mediated signaling.

214 he inter-domain twist to initiate and direct arrestin-mediated signaling.

215 ng as a therapeutic approach to control beta-arrestin-mediated signaling.

216 tinct receptor conformation to initiate beta-arrestin-mediated signaling.

217 directing signaling toward G-protein or beta-arrestin pathways.

218 IP6 binds to the arrestin phosphate sensor, and is stabilized by trimeriz

219 Arrestin plays another important signaling function.

220 the GLP-1 thiopeptides have much lower beta-arrestin potency, making them novel agonists with altere

221 hencyclidine, displayed a selective D2R/beta-arrestin potentiation of locomotion.

222 phorylation of the receptor and unbinding of arrestin, processes that are poorly understood.

223 of also altering CB1R interactions with beta-arrestin proteins that interact with the CB1R at the C-t

224 To further confirm the key role of beta-arrestin proteins, we overexpressed beta-arrestin2-(1-32

225 ell intrinsic physiology dependent upon beta-arrestin rather than G proteins.

226 the calcium flux assay while showing no beta-arrestin recruitment activity, is the most functionally

227 ounds with clear potency differences in beta-arrestin recruitment and G protein alpha i subunit (G al

228 dies demonstrate the role Ser-346/7 plays in arrestin recruitment and initiation of receptor desensit

229 CXCL11 induced CXCR3B-mediated beta-arrestin recruitment and little ERK phosphorylation.

230 played a 180-fold higher potency in the beta-arrestin recruitment assay (EC50 0.9 nM) compared with t

231 tion of G proteins (preferably Go) over beta-arrestin recruitment at dopamine D2 receptors.

232 lective 5-HT2C agonists possessing weak beta-arrestin recruitment can produce distinct receptor desen

233 iated, KOPR phosphorylation followed by beta-arrestin recruitment desensitized U50,488H-induced ERK1/

234 Arrestin recruitment did not correlate with scavenging;

235 selectively activate G-proteins versus beta-arrestin recruitment in D2R-BRET functional assays.

236 potency in both G alphai signaling and beta-arrestin recruitment is mandatory and this translates in

237 showed that although a high potency in beta-arrestin recruitment is required to fully internalize S1

238 , ECL residues mediate secondary binding and arrestin recruitment potency.

239 small-molecule-based screening using a beta-arrestin recruitment screening approach (PRESTO-Tango).

240 PAR4-P2Y12 heterodimer is necessary for beta-arrestin recruitment to endosomes and Akt signaling and

241 rodimer internalization is required for beta-arrestin recruitment to endosomes and Akt signaling.

242 K118A(3.26) in ECL1 showed moderate baseline arrestin recruitment with ablation of ligand-induced res

243 eadouts are radioligand binding competition, arrestin recruitment, and chemokine scavenging.

244 r(350) and Ser(349) are not necessary for ss-arrestin recruitment, but are involved in the stabilizat

245 s in stimulation of cAMP production and beta-arrestin recruitment, but for some replacement sets cAMP

246 We here show chemokine specificity in arrestin recruitment, by different effects of single ami

247 for Gq-mediated signaling compared with beta-arrestin recruitment.

248 s with apparent pathway selectivity for beta-arrestin recruitment.

249 ction is more strongly affected than is beta-arrestin recruitment.

250 o be critical for achieving bias toward beta-arrestin recruitment.

251 otein-independent ACKR3 responses and prompt arrestin recruitment.

252 units, adenylyl cyclase inhibition, and beta arrestin recruitment.

253 suppressing potency and efficacy toward beta-arrestin recruitment.

254 Gi biased agonist for KOR with minimal beta-arrestin recruitment.

255 degrade CXCL11 was not caused by the lack of arrestin recruitment; rather, arrestin was entirely disp

256 mediated GFP-CB1R as well as endogenous beta-arrestin redistribution to punctae, and conversely, CRIP

257 conversely, CRIP1a knockdown augmented beta-arrestin redistribution to punctae.

258 In contrast, when transiently bound, beta-arrestin reduces ERK activity via recruitment of a prote

259 time that Ang II receptor signaling to beta-arrestin regulates ARF6 activation.

260 for downstream trafficking and relies on the arrestin-related trafficking adaptor (ART)-Rsp5 ubiquiti

261 involves the Nedd4 ubiquitin ligase Rsp5 and arrestin-related trafficking adaptors (ARTs).

262 Arrestin-related trafficking proteins are important regu

263 had reduced CXCL11 scavenging despite intact arrestin responses.

264 (7.39) degraded chemokines in the absence of arrestin, S103D(2.63) had reduced CXCL11 scavenging desp

265 hen stably bound to phosphorylated M1R, beta-arrestin scaffolds and activates MEK-dependent ERK.

266 eferentially engage either G-protein or beta-arrestin signaling in 'indirect pathway' medium spiny ne

267 stly relies upon balanced G-protein and beta-arrestin signaling in iMSNs.

268 details of biased D2R/G-protein and D2R/beta-arrestin signaling in vivo has been challenging because

269 g the myofilament-Ca(2)(+) response via beta-arrestin signaling pathways.

270 kidney (HEK) cells, we demonstrate that beta-arrestin signaling plays a role in hERG regulation.

271 By disrupting this PAR4 calcium/beta-arrestin signaling process with a novel cell-penetrating

272 Ca(2)(+) response, we hypothesized that beta-arrestin signaling would increase myofilament-Ca(2)(+) r

273 at the cell surface control the magnitude of arrestin signaling, and therefore functional selectivity

274 Potential beta-arrestin signaling-mediated increases in hERG and IKr we

275 quire coordinated D2R/G-protein and D2R/beta-arrestin signaling.

276 side effects have mostly been linked to beta-arrestin signaling.

277 nes the ultimate cellular consequences of ss-arrestin signaling.

278 we test whether group I mGluRs require beta-arrestin signalling during specific forms of plasticity

279 binatorial interaction rules such that alpha-arrestins, stimulated via signaling cascades or in their

280 Recent evidence recognizes the beta-arrestin system as a key regulator of not only GPCRs, bu

281 eptide sequence permanently expose the alpha-arrestin-targeted region so that Art1 activation via TOR

282 ations induce active conformations of (beta-)arrestins that have recently been solved by X-ray crysta

283 GPCRs typically recruit arrestins through two different sets of interactions, on

284 f Ser-346/7 impaired the recruitment of beta-arrestin to CXCR4.

285 ization was required for recruitment of beta-arrestin to endocytic vesicles, which was dependent on c

286 othesized could attenuate the action of beta-arrestin to mediate CB1R internalization.

287 osphorylated by protein kinases and bound by arrestin to trigger desensitization and endocytosis.

288 different combinations of G-proteins or beta-arrestins to trigger specific downstream pathways.

289 receptor, and it reverses within seconds of arrestin unbinding from the transient binding mode.

290 ted ERK1/2 phosphorylation mediated via beta-arrestin unlike the orthosteric CP55,940 that does so in

291 e-based motif and occurs independent of beta-arrestins, unlike most classical GPCRs.

292 by the lack of arrestin recruitment; rather, arrestin was entirely dispensable for scavenging of eith

293 ns and/or scaffolding proteins, such as beta-arrestin, we find that the effects of D2Rs on prefrontal

294 al cytosolic tail targeted by the Art1 alpha-arrestin, which is activated via the TORC1 kinase comple

295 ERK1/2-RSK3 signaling, mediated through beta-arrestin, which may have a novel role in increasing MLC2

296 es, being equally efficacious on Gq and beta-arrestin, while Val(3)Pro(8)OXT showed reduced relative

297 e signaling in part through interaction with arrestins, whose binding promotes receptor internalizati

298 we investigate both the interaction of beta-arrestin with GPCRs, and the beta-arrestin conformationa

299 that tracks the dynamics of interactions of arrestin with receptors and of ERK activation using opti

300 th of the interactions of G-proteins or beta-arrestins with the corresponding active conformation pot