ライフサイエンスコーパス: beta-arrestin

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

2 ough its phosphorylated C-terminal tail with beta-arrestin.

3 llular binding partners (IBPs), e.g., Gs and beta-arrestin.

4 through the multifunctional adapter protein beta-arrestin.

5 )OXT showed reduced relative efficacy toward beta-arrestin.

6 ing cascades are controlled by G proteins or beta-arrestins.

7 ly, but nonexclusively, either G-proteins or beta-arrestins.

8 ing and activation process between GPCRs and beta-arrestins.

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

10 iggered by interactions of the receptor with beta-arrestins.

11 second wave (>5 minutes) that is mediated by beta-arrestins.

12 -II (AngII), including the Gq/11 protein and beta-arrestins.

13 governs the structural rearrangements within beta-arrestins.

14 ular loop (V2R(DeltaICL3)) can interact with beta-arrestin 1 (betaarr1) only through the phosphorylat

15 rimeric G proteins and the scaffold proteins beta-arrestin 1 and 2.

16 dentify the interaction kinetics of CB1R and beta-arrestin 1 during their endocytic trafficking as di

17 strate that ERK1/2 activation is mediated by beta-arrestin 1 from receptors localized exclusively at

18 Adult mice lacking beta-arrestin 1 selectively in hepatocytes did not show

19 rminal peptide competed for association with beta-arrestin 1, and phosphorylated central or distal C-

20 Our data reveal beta-arrestin 1, beta-arrestin 2, and AT1R as key regula

21 -dependent myofilament Ca(2+) sensitivity in beta-arrestin 1, beta-arrestin 2, and AT1R knockout mice

22 ive hemodynamics, we found that mice lacking beta-arrestin 1, beta-arrestin 2, or AT1R were unable to

23 etromer complex as a gatekeeper, terminating beta-arrestin 1-mediated ERK phosphorylation.

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

25 With its phosphate-binding concave surface, beta-arrestin-1 'reads' the message in the receptor phos

26 with nicotine led to enhanced recruitment of beta-arrestin-1 and E2F1 on vimentin, fibronectin, and Z

27 -P1 peptide to block the interaction between beta-arrestin-1 and PLCgamma abolishes TRV120027-induced

28 phospho-barcodes are translated to specific beta-arrestin-1 conformations and direct selective signa

29 hrin recognizes and stabilizes GRK2-specific beta-arrestin-1 conformations.

30 ether, these studies reveal a novel role for beta-arrestin-1 in the growth and metastasis of NSCLC.

31 beta-arrestin-1 knockdown or KO had no effect on signali

32 s and murine airways/whole animal subject to beta-arrestin-1 or -2 knockdown or knockout (KO).

33 We sought to determine the effect of beta-arrestin-1 or beta-arrestin-2 inhibition or gene ab

34 beta-Arrestin-1 promoted the expression of the mesenchym

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

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

37 Replacing the C-terminal region of beta-arrestin-1 with its counterpart on beta-arrestin-2

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

39 hosphorylated vasopressin-2 receptor tail to beta-arrestin-1.

40 were equally effective at coupling to Gi and beta-arrestin-1.

41 Here we demonstrate an active role of beta-arrestin 2 (Arrb2) in regulating spinal cord NMDA r

42 t that strategies aimed at enhancing hepatic beta-arrestin 2 activity could prove useful for suppress

43 ips, which steer the ligand bias between the beta-arrestin 2 and G protein pathway.

44 on inside Ift27(-/-) cilia and revealed that beta-arrestin 2 and the viral receptor CAR are candidate

45 We identified beta-arrestin 2 as the target gene of miR-365 by bioinfo

46 s confirmed with a NanoLuc Binary Technology beta-arrestin 2 assay, imaging of green fluorescent prot

47 otein-tagged beta-arrestin 2, and PathHunter beta-arrestin 2 assay.

48 y increased the activation of G proteins and beta-arrestin 2 by J113863.

49 However, hepatocyte-specific beta-arrestin 2 deficiency did not affect hepatic insuli

50 antly, hepatocyte-specific overexpression of beta-arrestin 2 greatly reduced hepatic GCGR signaling a

51 n contrast, knockdown or genetic ablation of beta-arrestin 2 in an insulin-secreting cell line and mo

52 inactivation of the GPCR-associated protein beta-arrestin 2 in hepatocytes of adult mice results in

53 n of exon 7-associated C-terminal tails with beta-arrestin 2 in morphine-induced desensitization and

54 ses morphine tolerance through regulation of beta-arrestin 2 in rats.

55 hifted the bias of several mu opioids toward beta-arrestin 2 over G protein activation compared with

56 f miR-365 caused a decrease in expression of beta-arrestin 2 protein.

57 nd leads to receptor internalization and the beta-arrestin 2 recruitment with potency comparable to t

58 Both in G protein-mediated pathways and in beta-arrestin 2 recruitment, no ligand-independent activ

59 failed to induce receptor internalization or beta-arrestin 2 recruitment.

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

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

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

63 of morphine tolerance through regulation of beta-arrestin 2, and miR-365 upregulation provides a pro

64 imaging of green fluorescent protein-tagged beta-arrestin 2, and PathHunter beta-arrestin 2 assay.

65 discover that excessive Krz, the Drosophila beta-arrestin 2, inhibits Smo sumoylation and prevents S

66 we found that mice lacking beta-arrestin 1, beta-arrestin 2, or AT1R were unable to generate a Frank

67 CCR2 or CCR5 also induced the recruitment of beta-arrestin 2, whereas UCB35625 did not.

68 Long-term beta-arrestin 2-biased agonism of the angiotensin II rec

69 -E54K) for 3 months with either TRV120067, a beta-arrestin 2-biased ligand of the angiotensin II rece

70 str3 ciliary localization in neurons lacking beta-arrestin 2.

71 ffects on recruitment of the adapter protein beta-arrestin 2.

72 minal peptides competed for association with beta-arrestin 2.

73 calcium responses were profoundly reduced in beta-arrestin-2 (barr2) deficient beta-cells.

74 Knockout of beta-arrestin-2 (betaarr-2(-/-)) attenuates the asthma p

75 coupled receptor kinase 5, thereby inducing beta-arrestin-2 biased PAR1 signaling by both APC and th

76 naling by thrombin, APC induces a protective beta-arrestin-2 biased PAR1 signaling by unknown mechani

77 main of protein C/APC is responsible for the beta-arrestin-2 biased PAR1 signaling independent of the

78 ructs revealed that EPCR occupancy initiates beta-arrestin-2 biased PAR1 signaling independent of the

79 , thrombin exerts cytoprotective effects via beta-arrestin-2 biased PAR1 signaling.

80 r of PI3K, and small interfering RNA against beta-arrestin-2 blocked C5a-induced adhesion.

81 protein, Gs, is greater in females, whereas beta-arrestin-2 coupling is greater in males.

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

83 The PAR1-dependent recruitment of beta-arrestin-2 in response to LPS by both APC and throm

84 o determine the effect of beta-arrestin-1 or beta-arrestin-2 inhibition or gene ablation on signaling

85 n of beta-arrestin-1 with its counterpart on beta-arrestin-2 or using a specific TAT-P1 peptide to bl

86 ed with in vitro kinase assays revealed that beta-arrestin-2 phosphorylation on Ser14 and Thr276 is e

87 0.34 +/- 0.01 hours for adrenaline-mediated beta-arrestin-2 recruitment and GFP-beta2 internalizatio

88 show a strong, predominantly NTS1R-mediated beta-arrestin-2 recruitment at the D2R/NTS1R-coexpressin

89 he slower rate for C26 resulted in levels of beta-arrestin-2 recruitment increasing up to 4-hour agon

90 sequently represent biased agonists favoring beta-arrestin-2 recruitment over canonical G protein act

91 nous ligand adrenaline in cAMP accumulation, beta-arrestin-2 recruitment, and receptor internalizatio

92 ined with other functional readouts, such as beta-arrestin-2 recruitment, cAMP accumulation, and calc

93 exceptional selectivity for muOR and minimal beta-arrestin-2 recruitment.

94 ator of MOR-induced G-protein signaling over beta-arrestin-2 recruitment.

95 and murine model systems, knockdown or KO of beta-arrestin-2 relative to control missense small inter

96 t with Gs-dependent signaling in females and beta-arrestin-2 signaling in males.

97 hat binds to APJ, activates the Galphai1 and beta-arrestin-2 signaling pathways, and induces receptor

98 ivation of M3-Rs inhibits the recruitment of beta-arrestin-2 to ORs, resulting in a potentiation of o

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

100 the mu opioid receptor but failed to recruit beta-arrestin-2, which is associated with opioid side ef

101 demonstrates that C5aR2 ligation initiates a beta-arrestin-2-, PI3K-, and ERK-dependent signaling pat

102 Similar to APC, thrombin triggered beta-arrestin-2-dependent recruitment of disheveled 2 (D

103 to biased signaling via either G proteins or beta-arrestin-2.

104 active state, leading to the recruitment of beta-arrestin-2.

105 late betaAR signaling preferentially through beta-arrestin, a concept known as beta-arrestin-biased a

106 common phenomenon among GPCRs, this mode of beta-arrestin activation may represent a novel mechanism

107 GPCR signalling is negatively regulated by beta-arrestins, adaptor molecules that also activate dif

108 ation of the PAR4-P2Y12 heterodimer promotes beta-arrestin and Akt co-localization to intracellular v

109 ems to involve scaffolding proteins, such as beta-arrestin and clathrin.

110 hare similar tertiary structure with visual-/beta-arrestins and also contains C-terminal PPXY motifs

111 provide new insights into the activation of beta-arrestins and reveal their novel role in receptor c

112 ain, which reduces PI4P binding and recruits beta-arrestins and the clathrin adaptor AP2 to trigger P

113 R4 internalization occurred independently of beta-arrestins and the receptor's C-tail domain.

114 eceptor complexes composed of a single GPCR, beta-arrestin, and G protein.

115 ctant-scavenging receptor, does not activate beta-arrestins, and is widely expressed by many leukocyt

116 al C-terminus, which was responsible for the beta-arrestin- and GPCR kinase-dependent endocytosis of

117 (beta-)Arrestins are important regulators of G-protein-co

118 mma-subunit (Gbetagamma), GPCR-kinase 2, and beta-arrestin are central to various cardiovascular dise

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

120 beta-arrestins are critical signalling molecules that re

121 tion of G protein-coupled receptors (GPCRs), beta-arrestins are essential scaffolds linking GPCRs to

122 As a result, G-proteins and beta-arrestins are in steric competition for binding to

123 beta-Arrestins are key regulators and signal transducers

124 lly favor responses by G-proteins, others by beta-arrestins, as has now been extensively studied.

125 gical concentrations of either G-proteins or beta-arrestins, as well as by phosphorylation or interac

126 In beta-arrestin assays, SARs were different, indicating bi

127 ere evaluated at the human GPR84 in cAMP and beta-arrestin assays.

128 using an unbiased G protein-coupled receptor-beta-arrestin-based screening and functional sensing sys

129 not only G(i/o)- but they can also influence beta-arrestin- (betaArr)-mediated signaling.

130 The beta-arrestins (betaarrs) are versatile, multifunctional

131 Beta-arrestins (betaarrs) critically mediate desensitiza

132 To understand the relative contribution of beta-arrestin bias to the efficacy of select beta-blocke

133 taAR ligand screened, nor is it required for beta-arrestin-bias activated by the beta2AR subtype of t

134 AR signaling and suggest that the concept of beta-arrestin-bias may need to be refined to incorporate

135 ly through beta-arrestin, a concept known as beta-arrestin-biased agonism.

136 ctive beta-blocker, has been classified as a beta-arrestin-biased agonist that can inhibit basal sign

137 at beta2AR expression is unaltered in CHF, a beta-arrestin-biased agonist that operates through the b

138 We previously discovered first-in-class beta-arrestin-biased agonists of dopamine D2 receptor (D

139 tility with volume loading, treatment with a beta-arrestin-biased AT1R ligand to selectively activate

140 ntially can be targeted therapeutically with beta-arrestin-biased AT1R ligands.

141 of beta2ARKO BM with rescued expression of a beta-arrestin-biased beta2AR in vivo restored BM CCR2 ex

142 efficacy of select beta-blockers, a specific beta-arrestin-biased pepducin for the beta2AR, intracell

143 s peptide agonist angiotensin II but not the beta-arrestin-biased peptide TRV120027.

144 cellular loop (ICL)1-9, was used to decouple beta-arrestin-biased signaling from occupation of the or

145 in recruitment, beta2AR internalization, and beta-arrestin-biased signaling.

146 In contrast, cannabinoids that are beta-arrestin-biased--such as THC found at high levels i

147 ear to regulate MOPr function: one affecting beta-arrestin binding and a second affecting agonist bin

148 mary phosphorylation cluster responsible for beta-arrestin binding and internalization.

149 beta-arrestin binding and the internalization kinetics o

150 Moreover, the stability of the beta-arrestin binding is a major determinant of the late

151 e associates with CRFR1; this is mediated by beta-arrestin binding motifs.

152 on of Smoothened, which by increasing Gpr161-beta-arrestin binding promotes Gpr161 removal, both duri

153 urements in living cells are consistent with beta-arrestin binding to M1 muscarinic acetylcholine rec

154 This suggests a competition for CRIP1a and beta-arrestin binding to the CB1R, which we hypothesized

155 We analyzed beta-arrestin binding, endocytosis, and subsequent traff

156 ssociates in complexes with either CRIP1a or beta-arrestin, but CRIP1a and beta-arrestin fail to coim

157 we demonstrate that Ang II receptors engage beta-arrestin, but not Gq, to mediate ARF6 activation in

158 ments in mouse embryonic fibroblasts lacking beta-arrestins combined with in vitro kinase assays reve

159 ary step for Erk recruitment to the receptor/beta-arrestin complex and Erk activation.

160 raction of beta-arrestin with GPCRs, and the beta-arrestin conformational changes in real time and in

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

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

163 ICL1-9 was also able to induce beta2AR- and beta-arrestin-dependent and Ca(2+)-independent contracti

164 1 expression, which itself was regulated via beta-arrestin-dependent beta2AR signaling.

165 urthermore, beta-blocker carvedilol-mediated beta-arrestin-dependent ERK activation is significantly

166 estin2 phosphorylation at Thr(383) underlies beta-arrestin-dependent Erk1/2 activation by GPCRs.

167 ise, Thr(383) phosphorylation is involved in beta-arrestin-dependent Erk1/2 stimulation elicited by o

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

169 receptors, which engage Erk1/2 pathway via a beta-arrestin-dependent mechanism, promotes MEK-dependen

170 Whether GPR40 engages beta-arrestin-dependent mechanisms and is subject to bia

171 ed receptors, signals through G-protein- and beta-arrestin-dependent pathways.

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

173 Converse to G-protein-dependent signaling, beta-arrestin-dependent signaling promotes cardiomyocyte

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

175 beta-Arrestins desensitize G protein signaling at DA rec

176 s on the mechanisms and cascades mediated by beta-arrestins downstream from the CB1R.

177 dent pathway but are weaker agonists for the beta-arrestin engagement and subsequent endocytosis towa

178 ther CRIP1a or beta-arrestin, but CRIP1a and beta-arrestin fail to coimmunoprecipitate with each othe

179 surface of either the G-protein-favoring or beta-arrestin-favoring GPCR conformation.

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

181 the mu-opioid receptor, which do not recruit beta-arrestin following receptor activation.

182 Thus, CRIP1a can compete with beta-arrestins for interaction with C-terminal CB1R doma

183 for the sustained binding between GPCRs and beta-arrestins, formed by phosphorylated serine-threonin

184 ) and the multifunctional transducer protein beta-arrestin have been shown to mediate mechanosensitiv

185 lathrin dependent and partially dependent on beta-arrestin in HEK293 cells, and nearly half of the in

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

187 localization and further suggest a role for beta-arrestin in the mediation of Sstr3 ciliary signalin

188 Together, our results implicate beta-arrestin in the modulation of Sstr3 ciliary localiz

189 e used to resolve the role of G proteins and beta-arrestins in D2R signaling assays.

190 Therefore, targeting beta-arrestins in PD L-DOPA therapy might prove to be a

191 preventing the recruitment of G proteins or beta-arrestins, in agreement with the lack of signalling

192 and CXCR4 receptors, but does not affect the beta-arrestin-independent Erk1/2 activation by 5-HT4 rec

193 ctivation pathways studied: cAMP production, beta-arrestin interaction, and MAP kinase activity.

194 bility lock not only stabilizes the receptor-beta-arrestin interaction, but also governs the structur

195 l motif that regulates calcium signaling and beta-arrestin interactions.

196 The interaction between receptors and beta-arrestins is generally believed to require both rec

197 Results from controlled expression of either beta-arrestin isoform demonstrate that beta-arrestin2 ac

198 ng abilities of IGF-1R to interact with each beta-arrestin isoform, depending on the presence of the

199 similar 3D structures, the widely expressed beta-arrestin isoforms 1 and 2 play at times identical,

200 Because the interplay between beta-arrestin isoforms governs the biological effects fo

201 demonstrates the antagonism between the two beta-arrestin isoforms in controlling IGF-1R expression

202 signaling, insensitive to pertussis toxin or beta-arrestin knock-out, and mimicked by Gs-DREADD stimu

203 ugh a previously unrecognized interaction of beta-arrestin localized to the sarcomere.

204 the purinergic receptor P2Y12 to coordinate beta-arrestin-mediated Akt signaling, an important media

205 ctivation of specific G-protein dependent or beta-arrestin-mediated cascade pathways.

206 ng at the plasma membrane, followed by rapid beta-arrestin-mediated desensitization and receptor inte

207 1R domains that could affect agonist-driven, beta-arrestin-mediated internalization of the CB1R.

208 1 and CXCL12 and signals exclusively through beta-arrestin-mediated pathways, without activating cano

209 NFAT is dependent on Galphaq/11-mediated or beta-arrestin-mediated signaling but rather involves lib

210 es constitute a comprehensive description of beta-arrestin-mediated signaling from CB1Rs and suggest

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

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

213 However, our current understanding of beta-arrestin-mediated signaling is still very limited.

214 ficking as a therapeutic approach to control beta-arrestin-mediated signaling.

215 a distinct receptor conformation to initiate beta-arrestin-mediated signaling.

216 kinases, and molecular mechanism underlying beta-arrestin-mediated signaling: We identify the intera

217 kinase signaling cascade activation, whereas beta-arrestin only activates elements of this cascade un

218 y the agonist, whereas the activation of the beta-arrestin pathway is linked to the stabilization of

219 pioid-receptor (muOR) signalling through the beta-arrestin pathway or by actions at other receptors.

220 D2R signals through distinct G-protein and beta-arrestin pathways, and drugs that are functionally

221 e by directing signaling toward G-protein or beta-arrestin pathways.

222 , but the GLP-1 thiopeptides have much lower beta-arrestin potency, making them novel agonists with a

223 ug, phencyclidine, displayed a selective D2R/beta-arrestin potentiation of locomotion.

224 as an interaction partner of the dishevelled-beta-arrestin protein complex by quantitative functional

225 proteins and the composition of dishevelled-beta-arrestin protein complexes contribute to the specif

226 thesized that the composition of dishevelled-beta-arrestin protein complexes contributes to signal sp

227 arrestin4), there are only two (non-visual) beta-arrestin proteins (beta-arrestin1 and beta-arrestin

228 able of also altering CB1R interactions with beta-arrestin proteins that interact with the CB1R at th

229 To further confirm the key role of beta-arrestin proteins, we overexpressed beta-arrestin2-

230 horylation of MOPr promotes association with beta-arrestin proteins, which then facilitates desensiti

231 and cell intrinsic physiology dependent upon beta-arrestin rather than G proteins.

232 o subunits, adenylyl cyclase inhibition, and beta arrestin recruitment.

233 on (as monitored via cAMP production) versus beta-arrestin recruitment (as monitored via BRET assays)

234 M in the calcium flux assay while showing no beta-arrestin recruitment activity, is the most function

235 ally selective compound (+)-7e produced weak beta-arrestin recruitment and also demonstrated less rec

236 PgammaS binding in mouse brain membranes and beta-arrestin recruitment and ERK phosphorylation in hCB

237 compounds with clear potency differences in beta-arrestin recruitment and G protein alpha i subunit

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

239 , displayed a 180-fold higher potency in the beta-arrestin recruitment assay (EC50 0.9 nM) compared w

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

241 The first step involves beta-arrestin recruitment by the signaling competent rec

242 at selective 5-HT2C agonists possessing weak beta-arrestin recruitment can produce distinct receptor

243 C-mediated, KOPR phosphorylation followed by beta-arrestin recruitment desensitized U50,488H-induced

244 cytoskeletal rearrangement or JWH133-induced beta-arrestin recruitment in cells transfected with eith

245 ds to selectively activate G-proteins versus beta-arrestin recruitment in D2R-BRET functional assays.

246 show that somatostatin treatment stimulates beta-arrestin recruitment into Sstr3-positive cilia and

247 high potency in both G alphai signaling and beta-arrestin recruitment is mandatory and this translat

248 s, we showed that although a high potency in beta-arrestin recruitment is required to fully internali

249 iased small-molecule-based screening using a beta-arrestin recruitment screening approach (PRESTO-Tan

250 heterodimer internalization is required for beta-arrestin recruitment to endosomes and Akt signaling

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

252 shedding, activation of NFAT luciferase, and beta-arrestin recruitment) but reduced activity relative

253 d by receptor binding, G protein activation, beta-arrestin recruitment, adenylyl cyclase inhibition,

254 was able to promote beta2AR phosphorylation, beta-arrestin recruitment, beta2AR internalization, and

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

256 phorylation and partial agonist activity for beta-arrestin recruitment, CXCL9 triggered only modest E

257 lators with apparent pathway selectivity for beta-arrestin recruitment.

258 production is more strongly affected than is beta-arrestin recruitment.

259 ars to be critical for achieving bias toward beta-arrestin recruitment.

260 cy at the G protein signaling pathway versus beta-arrestin recruitment.

261 neration as well as blunted GPCR kinases and beta-arrestin recruitment.

262 uced poor G protein coupling but substantial beta-arrestin recruitment.

263 g or suppressing potency and efficacy toward beta-arrestin recruitment.

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

265 ence for Gq-mediated signaling compared with beta-arrestin recruitment.

266 5940-mediated GFP-CB1R as well as endogenous beta-arrestin redistribution to punctae, and conversely,

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

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

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

270 They further indicate that beta-arrestins remain active after dissociation from rec

271 din-4, but exhibited a significantly reduced beta-arrestin response.

272 at, when stably bound to phosphorylated M1R, beta-arrestin scaffolds and activates MEK-dependent ERK.

273 at preferentially engage either G-protein or beta-arrestin signaling in 'indirect pathway' medium spi

274 2R mostly relies upon balanced G-protein and beta-arrestin signaling in iMSNs.

275 stic details of biased D2R/G-protein and D2R/beta-arrestin signaling in vivo has been challenging bec

276 ion of the individual roles of G-protein and beta-arrestin signaling pathways in D2R pharmacology, ne

277 tering the myofilament-Ca(2)(+) response via beta-arrestin signaling pathways.

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

279 n-biased AT1R ligand to selectively activate beta-arrestin signaling preserved the Frank-Starling rel

280 By disrupting this PAR4 calcium/beta-arrestin signaling process with a novel cell-penetr

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

282 Potential beta-arrestin signaling-mediated increases in hERG and I

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

284 ng require coordinated D2R/G-protein and D2R/beta-arrestin signaling.

285 Here we test whether group I mGluRs require beta-arrestin signalling during specific forms of plasti

286 Recent evidence recognizes the beta-arrestin system as a key regulator of not only GPCR

287 truncations induce active conformations of (beta-)arrestins that have recently been solved by X-ray

288 ion of Ser-346/7 impaired the recruitment of beta-arrestin to CXCR4.

289 ernalization was required for recruitment of beta-arrestin to endocytic vesicles, which was dependent

290 e hypothesized could attenuate the action of beta-arrestin to mediate CB1R internalization.

291 d by different combinations of G-proteins or beta-arrestins to trigger specific downstream pathways.

292 nstrated ERK1/2 phosphorylation mediated via beta-arrestin unlike the orthosteric CP55,940 that does

293 rosine-based motif and occurs independent of beta-arrestins, unlike most classical GPCRs.

294 orm at receptors that interact strongly with beta-arrestins via a C-terminal tail containing clusters

295 roteins and/or scaffolding proteins, such as beta-arrestin, we find that the effects of D2Rs on prefr

296 n of ERK1/2-RSK3 signaling, mediated through beta-arrestin, which may have a novel role in increasing

297 or-specific activation/deactivation cycle of beta-arrestins, which permits their active signalling.

298 rofiles, being equally efficacious on Gq and beta-arrestin, while Val(3)Pro(8)OXT showed reduced rela

299 Here we investigate both the interaction of beta-arrestin with GPCRs, and the beta-arrestin conforma

300 trength of the interactions of G-proteins or beta-arrestins with the corresponding active conformatio