ライフサイエンスコーパス: beta-arrestin

1 However, CysLTR2-L129Q only poorly recruits beta-arrestin.

2 us of PSMalpha2 in promoting FPR2 to recruit beta-arrestin.

3 xin-sensitive G protein but did not activate beta-arrestin.

4 nstream cellular responses via G proteins or beta-arrestin.

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

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

7 through the multifunctional adapter protein beta-arrestin.

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

9 is predicted to affect its interactions with beta-arrestin.

10 ased ability to signal via either Galphas or beta-arrestin.

11 ch for regulating receptor interactions with beta-arrestin.

12 the selective activation of G protein versus beta-arrestin.

13 signaling, with no measurable recruitment of beta-arrestin.

14 ependent pathways mediated by G proteins and beta-arrestins.

15 activate pathways mediated by G proteins or beta-arrestins.

16 upling to Galpha(s), but not to Galpha(q) or beta-arrestins.

17 the receptor increasingly unable to recruit beta-arrestins.

18 processes via heterotrimeric G proteins and beta-arrestins.

19 by linked G-proteins and the recruitment of beta-arrestins.

20 governs the structural rearrangements within beta-arrestins.

21 or 1 (NTSR1) in complex with truncated human beta-arrestin 1 (betaarr1(DeltaCT)).

22 sent a cryo-electron microscopy structure of beta-arrestin 1 (betaarr1) in complex with M2 muscarinic

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

24 or by GPCR kinases (GRKs) and by coupling of beta-arrestin 1 (betaarr1, also known as arrestin 2), wh

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

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

27 and skeletal muscle hypertrophy were lost in beta-arrestin 1 knockout mice, implying that arrestins,

28 kinase A inhibition by H-89 and knockdown of beta-arrestin 1 or beta-arrestin 2 did not affect the de

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

30 in the beta(1)-adrenoceptor in complex with beta-arrestin 1 versus a G protein-mimicking nanobody.

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

32 s, however, caused G-protein-independent but beta-arrestin 1-dependent phosphorylation of the downstr

33 e in skeletal muscle and this is mediated by beta-arrestin 1.

34 gnals via G proteins of all four classes and beta-arrestin 1.

35 nctional studies (Ca(i)(2+) mobilization and beta-arrestin 1/2 recruitment).

36 Beta-arrestin-1 and -2 (Barr1 and Barr2, respectively) a

37 aling but were fully competent in recruiting beta-arrestin-1 and -2.

38 ation assays in A549 cells, we observed that beta-arrestin-1 and unliganded GR interact in the cytopl

39 The GR/beta-arrestin-1 interaction uncovered here may help unra

40 These results demonstrate that beta-arrestin-1 is a crucial player for the stability of

41 We show that siRNA-mediated beta-arrestin-1 knockdown alters GR protein turnover by

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

43 tates of a phospho-beta2 adrenergic receptor/beta-arrestin-1(beta-arr1) membrane protein signaling co

44 tion between the glucocorticoid receptor and beta-arrestin-1, a scaffold protein with a well-establis

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

46 The enhanced GR turnover observed in beta-arrestin-1-deficient cells limits the duration of t

47 rapidly internalized on codeine binding in a beta-arrestin-1-dependent manner.

48 thways and is dependent on signaling via the beta-arrestin-1/2 and Ras homolog family member A (RhoA)

49 lation of ERK1/2 in cells that are devoid of beta-arrestin-1/2.

50 Here we report that beta-arrestin 2 (beta-Arr2), a canonical GPCR signaling

51 ts of IFN signaling remained intact, despite beta-arrestin 2 activation, as IFN-beta, IFN-gamma, IFN-

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

53 We identify beta-arrestin 2 as a key modulator of type I IFN in prim

54 In summary, we identify a novel role of beta-arrestin 2 as an integral regulator of type I IFN t

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

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

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

58 Small interfering RNA knockdown of beta-arrestin 2 demonstrated its role in IFNAR1 internal

59 by H-89 and knockdown of beta-arrestin 1 or beta-arrestin 2 did not affect the decreased cAMP produc

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

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

62 alization of the receptor and recruitment of beta-arrestin 2 in human embryonic kidney cell line 293

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

64 ression of a dominant negative dynamin 1 and beta-arrestin 2 knockdown had no effect, we concluded th

65 Similar effects of beta-arrestin 2 on IFN signaling occurred in hepatocytes

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

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

68 beta-Arrestin 2 was selectively activated by CCL2/CCR2 s

69 exhibited improved functional potency (cAMP, beta-arrestin 2), metabolic stability, and aqueous solub

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

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

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

73 RK signaling through ligand-independent, but beta-arrestin 2-dependent mechanisms.

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

75 e report the novel finding that mice lacking beta-arrestin-2 (barr2) selectively in adipocytes show s

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

77 nt of agonists biased against recruitment of beta-arrestin-2 could provide analgesic efficacy with fe

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

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

80 The intracellular scaffold protein beta-arrestin-2 is implicated in tolerance, hyperalgesia

81 In contrast, ECD-scFvhFc potently inhibits beta-arrestin-2 recruitment after PTH (1-34)-driven rece

82 ndent ERK1/2 phosphorylation, in addition to beta-arrestin-2 recruitment and downstream arrestin-depe

83 ced phosphorylation of FFA4-L and subsequent beta-arrestin-2 recruitment and extracellular-signal reg

84 pha(s), while they only show weak or even no beta-arrestin-2 recruitment at both beta(1)- and beta(2)

85 or G(q) protein activation and in particular beta-arrestin-2 recruitment at OX1R.

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

87 CXCR4-associated effects on thrombin-induced beta-arrestin-2 recruitment to and signaling of PAR1 cou

88 4 reduced the efficacy of thrombin to induce beta-arrestin-2 recruitment to recombinant PAR1 and enha

89 increase in KOR levels was also observed in beta-arrestin-2-deficient mice, highlighting the importa

90 nsible for recruitment and interactions with beta-arrestin-2.

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

92 beta-Arrestin, a molecular sensor of activated GPCRs, an

93 However, compound 48/80 induced a robust beta-arrestin activation as determined by transcriptiona

94 e findings indicate that NTSR1 G protein and beta-arrestin activation produce discrete and separable

95 Codeine-triggered beta-arrestin activation was also established by the Tan

96 protein signaling, but they can also induce beta-arrestin activation, leading to such side effects a

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

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

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

100 alpha peptides lacked the ability to recruit beta-arrestin and induce neutrophil chemotaxis, supporti

101 G protein signaling to a greater extent than beta-arrestin and internalization signaling pathways.

102 sults are consistent with the involvement of beta-arrestin and suggest that these allosteric modulato

103 GPCRs, but the functional interplay between beta-arrestin and the BBSome remains elusive.

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

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

106 with large bias factors toward G protein or beta arrestin are required for investigating the transla

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

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

109 differential engagement of G proteins versus beta-arrestins are commonly limited by the small respons

110 beta-arrestins are critical signalling molecules that re

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

112 beta-Arrestins are major regulators of G protein-coupled

113 For example, multifunctional beta-arrestin (ARRB) adapter proteins are best known as

114 signaling 2, RGS2; GPCR Kinase 5, GRK5; and beta-arrestin, Arrb2) using RT-PCR, qPCR, and western bl

115 ations in GPCR internalization and implicate beta-arrestin as a potential player mediating behavioral

116 ing a possible switch in coupling of D2Rs to beta-arrestin, as seen previously in a DYT1 model.

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

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

119 tivation of ACE2, agonism of MAS1 receptors, beta-arrestin-based Angiotensin receptor agonists, and a

120 embrane and are subsequently desensitized by beta-arrestin (beta-arr).

121 ein-coupled receptor (GPCR) family and binds beta-arrestins (beta-arrs), which regulate AT1R signalin

122 itiate signaling cascades via G-proteins and beta-arrestins (betaarr).

123 ) subfamily of heterotrimeric G-proteins and beta-arrestins (betaarrs) following C5a stimulation.

124 d binding to multifunctional proteins called beta-arrestins (betaarrs).

125 tin-biased agonist but also extends profound beta-arrestin bias to the endogenous ligand by selective

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

127 ulations to determine how fentanyl, a potent beta-arrestin biased agonist, binds the mu-opioid recept

128 ide molecular insight into fentanyl mediated beta-arrestin biased signaling and a rational framework

129 This small molecule not only acts as a beta-arrestin-biased agonist but also extends profound b

130 beta-arrestin-biased agonists deficient in Gq coupling d

131 nist angiotensin II (AngII) and two strongly beta-arrestin-biased analogs.

132 ch has been suggested to be an intrinsically beta-arrestin-biased GPCR.

133 , and has been demonstrated to function as a beta-arrestin-biased ligand for the beta(2)AR, stimulati

134 Harnessing beta-arrestin-biased MC4R signaling may represent an eff

135 n this issue of Cell, Slosky et al. report a beta-arrestin-biased neurotensin receptor ligand that ma

136 the cell surface activates cancer-protective beta-arrestin-biased signaling (beta-arr-BS).

137 t opioid peptides that efficaciously recruit beta-arrestin, bilorphin is G protein biased, weakly pho

138 Furthermore, mutagenesis of a beta-arrestin binding domain (Ala-Ser-Lys) within the in

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

140 erized (i.e., C-terminal phosphorylation and beta-arrestin binding), but a detailed analysis of melan

141 conformations that are capable of activating beta-arrestin but not heterotrimeric G(q) protein signal

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

143 PAR(2) coupling to Galpha(q), Galpha(s), and beta-arrestins, cathepsin-S (CS) and neutrophil elastase

144 e of 5-HT(2)R endocytic machinery, including beta-arrestin, clathrin, AP2, and dynamin, significantly

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

146 APK activation as well as endosomal receptor-beta-arrestin complex stabilization in the mitogenic res

147 opioid peptide DAMGO require M153 to induce beta-arrestin coupling, while M153 was dispensable for G

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

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

150 m-sensing receptor (CaSR) internalization is beta-arrestin-dependent and sensitive to modulation by a

151 biased ligand for the beta(2)AR, stimulating beta-arrestin-dependent but not G protein-dependent sign

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

153 es was greatly reduced, leading to decreased beta-arrestin-dependent ERK1/2 activation, faster recycl

154 beta-arrestin-dependent ERK1/2 regulation is the subject

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

156 on of AT1R by angiotensin II (ANGII) elicits beta-arrestin-dependent inhibition and internalization o

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

158 cium imaging, phosphate radiolabeling, and a beta-arrestin-dependent luciferase assay, we characteriz

159 chains comprising K63 linkages (UbK63) in a beta-arrestin-dependent manner before BBSome-mediated ex

160 riggers cell membrane blebbing in a RhoA-and beta-arrestin-dependent manner.

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

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

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

164 l could enhance skeletal muscle strength via beta-arrestin-dependent pathways.

165 at dictates non-GPCR interactions specifying beta-arrestin-dependent signaling by a GPCR.

166 d significantly lower receptor upregulation (beta-Arrestin-dependent signaling pathway) upon stimulat

167 the activation of both their G protein- and beta-arrestin-dependent signaling pathways.

168 ellularly in ligand naive cells, yet exhibit beta-arrestin-dependent signaling responses, mitogen-act

169 To study the link between beta-arrestin-dependent trafficking and ERK1/2 signaling

170 elling evidence that CaSR internalization is beta-arrestin-dependent while interestingly being largel

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

172 Additionally, beta-arrestin directly regulates many cell signalling pa

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

174 of abuse, the effect of alcohol exposure on beta-arrestin expression and beta-arrestin-mediated GPCR

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

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

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

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

179 nd blocking the recruitment and signaling of beta-arrestin in response to ghrelin.

180 rough distinct noncanonical pathways such as beta-arrestins in addition to the canonical G protein-de

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

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

183 re temporally correlated with increased GPCR/beta-arrestin interaction signals in response to agonist

184 s that occur later than agonist-induced GPCR/beta-arrestin interaction signals, indicating that GPCR/

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

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

187 ternalization and infection, suggesting that beta-arrestin interactions with 5-HT(2A)R are critical f

188 ng AT1R variants that show distinct receptor-beta-arrestin interactions: A163T, T282M, and C289W.

189 beta-Arrestin is a key player involved in the regulation

190 the mu-opioid receptor and interaction with beta-arrestins is controlled by carboxyl-terminal phosph

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

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

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

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

195 veal that PX exploits the antagonism between beta-arrestin isoforms; in low ligand conditions, PX fav

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

197 Although beta-arrestin levels are influenced by various drugs of

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

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

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

201 AT1-B2 receptor aggregation was inhibited by beta-arrestin-mediated downregulation.

202 for Gq/11 signaling pathways while escaping beta-arrestin-mediated downregulation.

203 hol exposure on beta-arrestin expression and beta-arrestin-mediated GPCR trafficking is poorly unders

204 Thus, TAS2R14 is subject to beta-arrestin-mediated internalization and subsequent do

205 1R domains that could affect agonist-driven, beta-arrestin-mediated internalization of the CB1R.

206 cking and suggest conformationally dependent beta-arrestin-mediated MAPK activation as well as endoso

207 1 and CXCL12 and signals exclusively through beta-arrestin-mediated pathways, without activating cano

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

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

210 ed safety profiles are due to a reduction in beta-arrestin-mediated signaling or, alternatively, to t

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

212 attributed to the preferential activation of beta-arrestin over G proteins, make methadone a standard

213 ards the G protein-mediated pathway over the beta-arrestin pathway.

214 n, the effects of MRAP2 on the Galpha(q) and beta-arrestin pathways were independent and involved dis

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

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

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

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

219 -L phosphorylation, as well as DHA-dependent beta-arrestin recruitment and DHA-dependent extracellula

220 effects of loss of phosphorylation sites on beta-arrestin recruitment and ERK1/2 activation.

221 4R variants exhibiting signaling bias toward beta-arrestin recruitment and increased mitogen-activate

222 ion, and NADPH oxidase activity, yet lack of beta-arrestin recruitment and neutrophil chemoattraction

223 not the late phase generally associated with beta-arrestin recruitment and receptor endocytosis, prom

224 (2+)/calmodulin-dependent manner, preventing beta-arrestin recruitment and receptor internalization.

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

226 e conducted a high-throughput screen using a beta-arrestin recruitment assay.

227 dissociation kinetic measurements coupled to beta-arrestin recruitment assays to investigate ACKR3:ch

228 ing radioligand binding displacement assays, beta-arrestin recruitment assays, cyclic AMP inhibition

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

230 st receptors in close proximity, but impedes beta-arrestin recruitment by all receptors tested.

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

232 re unchanged or exacerbated, indicating that beta-arrestin recruitment does not contribute to the sev

233 receptor activation, G protein coupling, and beta-arrestin recruitment for all tested ligands.

234 nds were CCR2-selective, 39 and 43 inhibited beta-arrestin recruitment in CCR5 with high potency.

235 ficant bias toward G protein activation over beta-arrestin recruitment in comparison to quinpirole.

236 le: it preferentially and potently activated beta-arrestin recruitment in vitro and potently elicited

237 Because beta-arrestin recruitment is dependent on receptor phosp

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

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

240 hat the difference in G protein efficacy and beta-arrestin recruitment of the hybrid ( S)-22, the ful

241 n of protein kinase D (PKD) and PKA, but not beta-arrestin recruitment or PAR(2) endocytosis.

242 A/protein kinase D (PKD) activation, but not beta-arrestin recruitment or PAR(2) endocytosis.

243 C(50) ~ 2-6 nM) but minimally activating the beta-arrestin recruitment pathway (<=55% maximum signal

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

245 We found that the maximal efficacy of beta-arrestin recruitment to MC4R, rather than canonical

246 Agonists evoked beta-arrestin recruitment to TAS2R14, which was not seen

247 ate calcium signaling and is more potent for beta-arrestin recruitment triggered greater levels of pl

248 ations within other GPCRs similarly impaired beta-arrestin recruitment while maintaining G protein si

249 ing properties ([(35)S]GTPgammaS binding and beta-arrestin recruitment) of 22 peptides at each of the

250 n, cAMP inhibition, Ca(2+) mobilization, and beta-arrestin recruitment) which identified ERK1/2 phosp

251 pha(q/11)-coupled calcium-signaling pathway, beta-arrestin recruitment, and mitogen-activated protein

252 Despite the lack of beta-arrestin recruitment, the PSMalpha peptides induced

253 mulation, AT1R receptor phosphorylation, and beta-arrestin recruitment.

254 yclase inhibition, calcium mobilization, and beta-arrestin recruitment.

255 Galphas enhancers while minimally activating beta-arrestin recruitment.

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

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

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

259 vely coupled to receptor engagement, such as beta-arrestin recruitment.

260 mine receptor (D2R) that results in impaired beta-arrestin recruitment.

261 5940-mediated GFP-CB1R as well as endogenous beta-arrestin redistribution to punctae, and conversely,

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

263 horylation of the receptor or recruitment of beta-arrestin scaffolding proteins could preserve the an

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

265 induce G protein signaling without inducing beta-arrestin signaling can alleviate pain while reducin

266 attenuates G protein signaling and augments beta-arrestin signaling downstream of KOR, exhibiting co

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

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

269 heterotrimeric G protein signaling, whereas beta-arrestin signaling is considered central to their d

270 However, the mechanism for stimulating beta-arrestin signaling is not known, making it difficul

271 stand how their bias toward G-protein versus beta-arrestin signaling pathways is regulated.

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

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

274 , consistent with the augmented KOR-mediated beta-arrestin signaling seen upon RGS12 over-expression.

275 ficient mice, highlighting the importance of beta-arrestin signaling to establishing steady-state KOR

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

277 ced conditioned place aversion (considered a beta-arrestin signaling-dependent behavior), consistent

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

279 upling from canonical G(i/o) to noncanonical beta-arrestin signaling.

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

281 hat engages with effector molecules to drive beta-arrestin signaling.

282 What chemical features dictate G protein or beta-arrestin signaling?

283 Inhibition of clathrin or beta-arrestin specifically reduced JCPyV internalization

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

285 the n-aniline ring of fentanyl mediates muOR beta-arrestin through a novel M153 "microswitch" by synt

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

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

288 nonical activation of G proteins and engages beta-arrestins to mediate distinct cellular signaling ev

289 motaxis, supporting the previous notion that beta-arrestin translocation is of importance for cell mi

290 , ML417 (20), potently promotes D3R-mediated beta-arrestin translocation, G protein activation, and E

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

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

293 G-protein-coupled receptors (GPCRs) recruit beta-arrestin, which desensitizes heterotrimeric G-prote

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

295 GPCR) family, signals through G proteins and beta-arrestins, which act as adaptors to regulate AT1R i

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

297 suggest that the cooperative interactions of beta-arrestin with both the receptor and the phospholipi

298 ompound 48/80 signals via both G protein and beta-arrestin with distinct differences in receptor regu

299 lar mechanisms underlying the interaction of beta-arrestin with GPCRs are much less understood.

300 orylating the MOPr and marginally recruiting beta-arrestin, with no receptor internalization.