ライフサイエンスコーパス: beta-arrestin 2

1 inant-negative mutant version of arrestin-3 (beta-arrestin-2).

2 d be rescued by cotransfection of cells with beta-arrestin 2.

3 s and receptor trafficking were regulated by beta-arrestin 2.

4 sent in dorsal root ganglion neurons lacking beta-arrestin 2.

5 through either G-protein alpha subunit 12 or beta-arrestin 2.

6 dopamine-mediated interaction of D2(L)R with beta-arrestin 2.

7 he association between active Smoothened and beta-arrestin 2.

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

9 signaling is not inhibited in the absence of beta-arrestin 2.

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

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

12 dent (PPM/PP2C) family and is independent of beta-arrestin 2.

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

14 ient to confer MAPK sensitivity to the human beta-arrestin-2.

15 of a molecular complex composed of TRAF6 and beta-arrestin-2.

16 tion to dendritic spines that is mediated by beta-arrestin-2.

17 2) "protective" effects) were independent of beta-arrestin-2.

18 eta-arrestin-1 and repress the expression of beta-arrestin-2.

19 animals were not observed in animals lacking beta-arrestin-2.

20 ver, DOI invokes the behavior independent of beta-arrestin-2.

21 sts from mice lacking beta-arrestin-1 and/or beta-arrestin-2.

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

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

24 Here, we show in cells and mice that beta-arrestin 2, a central element in GPCR trafficking,

25 subtype showed the strongest sensitivity to beta-arrestin 2 action.

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

27 otaxis, G protein-dependent and independent (beta-arrestin-2) activation, or secondary chemokine (CCL

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

29 This suggests that deleting beta-arrestin 2 affects the JNK cascade.

30 WT mice revealed that lithium disrupted the beta-arrestin-2/Akt/PP2A complex by directly inhibiting

31 r loss of one copy of the Gsk3b gene reduced beta-arrestin-2/Akt/PP2A complex formation in mice, whil

32 Thus, GSK-3 regulates the stability of the beta-arrestin-2/Akt/PP2A complex, and lithium disrupts t

33 beta-arrestin-2/AKT/protein phosphatase 2A (beta-arrestin-2/AKT/PP2A) complex that is known to be re

34 s, glycogen synthase kinase-3 (GSK-3), and a beta-arrestin-2/AKT/protein phosphatase 2A (beta-arresti

35 ssical function in receptor desensitization, beta-arrestin 2 also acts as a signaling intermediate th

36 esonance energy transfer)-based biosensor of beta-arrestin 2 and a combination of biased ligands and/

37 -60 min was blocked by depletion of cellular beta-arrestin 2 and beta-arrestin 1 by small interfering

38 receptors and increased interaction between beta-arrestin 2 and ERK1/2.

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

40 beta-Arrestin 2 and GRK2 are thus potential mediators of

41 mulated a low level of TGR5 interaction with beta-arrestin 2 and GRK2.

42 signaling complex with the scaffold proteins beta-arrestin 2 and Ile Gln motif containing GTPase Acti

43 beta-arrestin 2 and iNOS coimmunoprecipitated, and there

44 un-N-terminal kinase (JNK), which binds with beta-arrestin 2 and modulates the analgesic effects of m

45 Tsai identify two very different molecules--beta-arrestin 2 and Par-4, respectively--that unexpected

46 , a prototypical GPCR, dissociates eNOS from beta-arrestin 2 and promotes binding of beta-arrestin 2

47 uggest that a functional interaction between beta-arrestin 2 and Smoothened may be critical to regula

48 ough the promotion of an association between beta-arrestin 2 and Smoothened.

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

50 linked calcium signaling pathway mediated by beta-arrestin-2 and ERK1/2.

51 te production by 48% (beta-arrestin-1), 71% (beta-arrestin-2), and 84% (beta-arrestins-1 and -2).

52 ed with beta-arrestin 1, 164 interacted with beta-arrestin 2, and 102 interacted with both beta-arres

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

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

55 nes derived from wild type, beta-arrestin 1, beta-arrestin 2, and beta-arrestin 1/2 knock-out mice.

56 p-regulation of GRK5 involves CB2 receptors, beta-arrestin 2, and ERK1/2 signaling because treatment

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

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

59 rupting a signaling complex composed of Akt, beta-arrestin 2, and protein phosphatase 2A.

60 (ERK) through a pathway mediated by dynamin, beta-arrestin 2, and Src.

61 tes with constitutive localization of PAR-2, beta-arrestin-2, and activated ERK1/2 to pseudopodia.

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

63 calcium, inhibited cAMP signaling, recruited beta-arrestin-2, and stimulated filamentous-actin accumu

64 sphorylation of the receptor, recruitment of beta-arrestin-2, and subsequent receptor internalization

65 on RAR beta2 transcriptional activation in a beta-arrestin 2- and ERK2-dependent manner.

66 1A (AT(1A)) receptor results in independent beta-arrestin 2- and G protein-mediated extracellular si

67 The nonvisual arrestins, beta-arrestin-1 and beta-arrestin-2, are multifunctional scaffolding protein

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

69 e characterize the conformational changes in beta-arrestin 2 (arrestin 3) by comparing the limited tr

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

71 amine-associated behaviors, thus implicating beta-arrestin 2 as a positive mediator of dopaminergic s

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

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

74 In this study, we identify beta-arrestin-2 as a scaffolding protein that regulates

75 oxy-4-iodoamphetamine (DOI), in mice lacking beta-arrestin-2, as well as in cells lacking beta-arrest

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

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

78 Mechanistically, we found that beta-arrestin 2 associated with CARMA3, a scaffold prote

79 ted with rapid and transient inhibition of a beta-arrestin 2-associated pool of protein phosphatase 2

80 We report beta-arrestin-2 association with TRPV1 in multiple cell

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

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

83 g either beta-arrestin 1 (beta arr1(-/-)) or beta-arrestin 2 (beta arr2(-/-)), agonist-induced DTS de

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

85 Using neurons lacking beta-arrestin 2 (beta-arr2-/-) to examine this interacti

86 beta-arrestin-2 (beta-arr2) is a scaffolding protein of

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

88 but not homologous) desensitization required beta-arrestin-2 (betaarr-2) because it was nearly abolis

89 We have previously shown that beta-arrestin-2 (betaarr2) depletion promotes CXCR2-medi

90 element binding protein (CREB) and elevated beta-arrestin-2 (betaarr2) expression.

91 e have previously shown that adaptor protein beta-arrestin-2 (betaarr2) plays a crucial role in trans

92 posed to NT, beta-arrestin-1 (betaARR1), and beta-arrestin-2 (betaARR2) translocate to early endosome

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

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

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

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

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

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

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

100 C3aR phosphorylation there was no change in beta-arrestin-2 binding or receptor desensitization.

101 s was associated with 74+/-2.4% decreases in beta-arrestin-2 binding, significantly reduced desensiti

102 omplete loss of receptor phosphorylation and beta-arrestin-2 binding.

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

104 In this work, we found that beta-arrestin 2, but not beta-arrestin 1, is required fo

105 R antagonist and in MFS mice lacking AT1R or beta-arrestin 2, but not in MFS mice treated with an ang

106 d 379) thereby enhancing clathrin binding to beta-arrestin 2 by 10-fold.

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

108 in why the analog promotes higher amounts of beta-arrestin 2.CCR5 complexes, thereby increasing CCR5

109 We find a novel role for MAPK in the B2R/beta-arrestin-2 complex formation, receptor trafficking

110 lieve to be a new link between GSK-3 and the beta-arrestin-2 complex in mice and propose an integrate

111 it with high constitutive activity, the CCR1.beta-arrestin-2 complex is required for G protein-indepe

112 okine by the receptor suggests that the CCR1.beta-arrestin-2 complex may be related to a potential sc

113 of the behavioral phenotypes of mice lacking beta-arrestin 2 could be a result of altered JNK signali

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

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

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

117 Although beta-arrestin 2 deficiency did not affect LPA-induced IK

118 beta-arrestin 2 deficiency in mice results in reduction

119 Smoothened, rescues the phenotypes caused by beta-arrestin 2 deficiency.

120 Because beta-arrestin-2-deficient (betaarr2(-/-)) mice exhibited

121 Moreover, beta-arrestin-2-deficient hippocampal neurons are resist

122 beta-Arrestin-2-deficient mice exhibit normal hippocampa

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

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

125 the PAR(2)-enhanced inflammatory process is beta-arrestin-2 dependent, whereas the protective antico

126 These findings demonstrated p38 MAPK- and beta-arrestin 2-dependent cross-regulation between neuro

127 cription of early growth response 1, whereas beta-arrestin 2-dependent ERK activation did not.

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

129 ences of ERK activation by the G protein and beta-arrestin 2-dependent pathways were also distinct.

130 ia both G protein-dependent and independent (beta-arrestin 2-dependent) signaling, but the role of th

131 erotonin induces a head twitch response by a beta-arrestin-2-dependent mechanism.

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

133 beta-Arrestin 1 or beta-arrestin 2 depletion prevented the localization of

134 ntly, inhibition of PDE4D5 activity reversed beta-arrestin-2 desensitization of TRPV1.

135 Hippocampal neurons lacking beta-arrestin-2 develop mature spines that fail to remod

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

137 dues of the RAR beta2 receptor through which beta-arrestin 2 effects are mediated.

138 he phosphorylation of CB2 receptors; and the beta-arrestin 2/ERK interactions.

139 In beta-arrestin 2 expressing cells, three of the seven LPA

140 dependent ERK1/2 activation, indicating that beta-arrestin 2 expression confers ERK1/2 activation via

141 ndent protein kinase 1 and instead relies on beta-arrestin 2 for assembly.

142 These data indicate that beta-arrestin 2 functions both to attenuate EGF receptor

143 (GRK2) leads to phosphorylation of Smo, and beta-arrestin 2 fused to green fluorescent protein inter

144 We identified elevated expression of the beta-arrestin 2 gene (Arrb2) in the striatum and the hip

145 d in vivo murine models, we demonstrate that beta-arrestin-2 gene ablation augments beta-agonist-medi

146 differentially regulate beta-arrestin-1 and beta-arrestin-2 gene expression in multiple cell types.

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

148 he beta-arrestin-1 gene and intron-11 of the beta-arrestin-2 gene.

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

150 py, the two mutant receptors interacted with beta-arrestin 2-green fluorescent protein with much lowe

151 In cells lacking beta-arrestin 2, >80% of LPA-stimulated ERK1/2 phosphory

152 Expression of beta-arrestin-2 had no effect on TSHR cAMP signaling, dy

153 Recently, beta-arrestin 2 has been shown to act as a signal mediat

154 Release of the C terminus from the rest of beta-arrestin 2 has functional consequences in that it i

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

156 In contrast, we show the critical role of beta-arrestin 2 in CB1 receptor internalization upon tre

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

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

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

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

161 mass spectrometry (MALDI-TOF MS) profiles of beta-arrestin 2 in the presence of a phosphopeptide (V(2

162 Thus, the V(2)R-pp can activate beta-arrestin 2 in vitro, most likely mimicking the effe

163 re, we show that the functional knockdown of beta-arrestin 2 in zebrafish embryos recapitulates the m

164 CCR1 concurrently engages Galphai and beta-arrestin-2 in a multiprotein complex, which may be

165 These findings establish a key role for beta-arrestin-2 in mediating cellular cytoprotective fun

166 Our studies demonstrate unique functions of beta-arrestin-2 in NMDAR-mediated dendritic spine and sy

167 Moreover, siRNA-mediated knockdown of beta-arrestin-2 in primary cultures resulted in a signif

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

169 8alpha, and AKT1, whereas down-regulation of beta-arrestin-2 increased phosphorylation of AKT1 in bot

170 n by the epidermal growth factor receptor (a beta-arrestin 2 independent pathway) had no effect on iN

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

172 Furthermore, beta-arrestin-2 inhibits C3a-induced NF-kappaB activatio

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

174 Thus, selective targeting of D2(L)R/beta-arrestin 2 interaction and related signaling pathwa

175 (PKA)-activated PDE4D3, scaffolded through a beta-arrestin 2 interaction with Ser(704) of the recepto

176 MP production and partial agonists for D(2)R/beta-arrestin-2 interactions.

177 Introducing FLAG epitope-tagged beta-arrestin 2 into the beta-arrestin 1/2 null backgrou

178 Beta-arrestin 2 is a multifunctional key component of th

179 e of the cascades that could be regulated by beta-arrestin 2 is cJun-N-terminal kinase (JNK), which b

180 nd NO-dependent shift in the affiliations of beta-arrestin 2 is followed by denitrosylation.

181 Furthermore, this function of beta-arrestin 2 is important for the expression of dopam

182 synthase (eNOS), and that S-nitrosylation of beta-arrestin 2 is promoted by endogenous S-nitrosogluth

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

184 ory motif is conserved between rat and mouse beta-arrestin-2, it is surprisingly not conserved in hum

185 PV1 desensitization in primary cultures from beta-arrestin-2 knock-out mice compared with wild type.

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

187 ion of Smoothened and GRK2, is diminished by beta-arrestin 2 knockdown with shRNA.

188 pendent ERK activation was also inhibited by beta-arrestin 2 knockdown.

189 When administered to beta-arrestin 2 knockout mice, lithium fails to affect A

190 lgesic response with reduced side effects in beta-arrestin-2 knockout mice compared to wild-type mice

191 n wild-type mice was completely abolished in beta-arrestin-2 knockout mice.

192 n E(2) receptors were not affected by either beta-arrestin-2 knockout or arrestin knockdown.

193 Overexpression of either beta-arrestin 1 or beta-arrestin 2 led to marked inhibition of NF-kappaB ac

194 nduced NF-kappaB activation, suggesting that beta-arrestin 2 may recruit CARMA3 to LPA receptors.

195 lar mechanism involving inhibition of D2(L)R/beta-arrestin 2 mediated signaling.

196 ent, but yet appeared exclusively to support beta-arrestin 2-mediated ERK activation.

197 to Gq/11, GPR40 is functionally linked to a beta-arrestin 2-mediated insulinotropic signaling axis.

198 oteins mediate thrombin's signaling, whereas beta-arrestin 2 mediates APC's signaling.

199 These data show that beta-arrestin 2 mediates B1R-dependent high-output NO by

200 Here we demonstrate that beta-arrestin-2 mediates anti-apoptotic cytoprotective s

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

202 cytokine production, and mucin production in beta-arrestin-2(-/-) mice.

203 TNFalpha, were enhanced in wild-type but not beta-arrestin-2(-/-) mice.

204 l migration are inhibited in leukocytes from beta-arrestin-2(-/-) mice.

205 Our results demonstrate that beta-arrestin 2 modulates acute responses to ethanol and

206 e cellular complement of beta-arrestin-1 and beta-arrestin-2 occur in many human diseases, and their

207 The proteolysis of beta-arrestin 2 occurs, but the pattern is more complex.

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

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

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

211 Expression of wild-type beta-arrestin 2, or constitutive activation of the Hh pa

212 horylation promotes receptor selectivity for beta-arrestin 2 over beta-arrestin 1.

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

214 or these effects is likely the non-canonical beta-arrestin-2 pathway.

215 pathway independently of the G-inhibitory or beta-arrestin-2 pathways.

216 2, it is surprisingly not conserved in human beta-arrestin-2 (PEK(178)P).

217 ulatory motif in the hinge domain of the rat beta-arrestin-2 (PET(178)P), but not rat beta-arrestin-1

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

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

220 Here we report that beta-arrestin-2 plays an important role in NMDA-induced

221 Studies in mice have shown that beta-arrestin-2 plays an important role in the developme

222 formation of signaling complexes containing beta-arrestin 2, PP2A, and Akt.

223 , we have recently shown that GRK2, GRK3 and beta-arrestin-2 promote C3a receptor (C3aR) desensitizat

224 n with unlabeled TSH; however, expression of beta-arrestin-2 promoted TSHR internalization that was i

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

226 We also demonstrated that beta-arrestin-2 provides an inhibitory signal for NF-kap

227 and ziprasidone all potently antagonize the beta-arrestin 2 recruitment to D2(L)R induced by quinpir

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

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

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

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

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

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

234 0.34 +/- 0.01 hours for adrenaline-mediated beta-arrestin-2 recruitment and GFP-beta2 internalizatio

235 Ser470 participate in C3aR desensitization, beta-arrestin-2 recruitment and inhibition of NF-kappaB

236 mine the role of receptor phosphorylation on beta-arrestin-2 recruitment and RBL-2H3 cells for functi

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

238 nt ligand bias for G-protein activation over beta-arrestin-2 recruitment at D(2S) receptors.

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

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

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

242 inct conformations of a 7TMR associated with beta-arrestin-2 recruitment or G-protein coupling and va

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

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

245 4 reduced the efficacy of thrombin to induce beta-arrestin-2 recruitment to recombinant PAR1 and enha

246 f Ca(2)(+) mobilization, beta-arrestin-1 and beta-arrestin-2 recruitment, and extracellular signal-re

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

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

249 azines (1,4-DAPs) behaved as antagonists for beta-arrestin-2 recruitment, implying significant ligand

250 AR and GRK-promoted events was identified by beta-arrestin-2 recruitment.

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

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

253 beta-Arrestin 2 reduced thyrotropin-releasing hormone (T

254 d dynamic S-nitrosylation/denitrosylation of beta-arrestin 2 regulates stimulus-induced GPCR traffick

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

256 ytosis, mediated by a novel interaction with beta arrestin-2, results in decreased TGF-beta signaling

257 In summary, removing beta-arrestin 2 reveals mu receptor activation of the JN

258 In addition, we found that beta-arrestin-2 scaffolding of phosphodiesterase PDE4D5

259 ur results provide the genetic evidence that beta-arrestin 2 serves as a positive regulator in NF-kap

260 Because beta-arrestin 2 serves to link CRF1 to Gs-independent si

261 ontaining protein tyrosine phosphatase 2 and beta-arrestin 2, showed higher inhibition of lipid raft

262 eatment with CB2 shRNA lentiviral particles, beta-arrestin 2 shRNA lentiviral particles, or ERK1/2 in

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

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

265 and suggest differential endosomal receptor/beta-arrestin-2 signaling roles among species.

266 Genetic deletion of beta-arrestin-2 simultaneously attenuated the antipsycho

267 n by the mutant receptors was insensitive to beta-arrestin 2 small interfering RNA but was reduced mo

268 h H89, an inhibitor of protein kinase A, and beta-arrestin 2 small interfering RNA, respectively.

269 in-dependent signaling, and are abrogated by beta-arrestin-2 small interfering RNA.

270 V(2)R-pp binds to beta-arrestin 2 specifically, whereas V(2)R-np does not.

271 Here, we report that beta-arrestin 2 stimulates the transcriptional activatio

272 not most other mu agonists, in mice lacking beta-arrestin 2, suggest that this scaffolding protein r

273 ted mutagenesis and cells or tissues lacking beta-arrestin 2 suggests a role for these desensitizatio

274 imetic residue in both the rat and the human beta-arrestin-2 (T/K178D) significantly stabilizes B2R/b

275 vasopressin V2 receptors was altered by the beta-arrestin-2 T178D mutant.

276 CRF receptor (CRF1) with the Gs protein and beta-arrestin 2 that would render females more responsiv

277 , we observed that in MEF cells deficient in beta-arrestin 2 the internalization of the beta2-adrener

278 ion events were abrogated after depletion of beta-arrestin 2 through siRNA-mediated knockdown.

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

280 from beta-arrestin 2 and promotes binding of beta-arrestin 2 to clathrin heavy chain/beta-adaptin, th

281 ed enhanced green fluorescent protein (EGFP)-beta-arrestin 2 to the plasma membrane, whereas the SA3

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

283 , benzamide 7b, that promotes recruitment of beta-arrestin-2 to the microOR and receptor internalizat

284 that 1c does not promote the recruitment of beta-arrestin-2 to the microOR or receptor internalizati

285 kinorin, does not promote the recruitment of beta-arrestin-2 to the muOR and does not lead to recepto

286 inase 1/2 phosphorylation and recruitment of beta-arrestin(2) to the membrane.

287 nhibition correlates with the formation of a beta-arrestin-2/TRAF6 complex.

288 To determine the contributions of beta-arrestin 2, transactivated EGF receptors, and ERK1/

289 Activation of beta-arrestin 2 upon V(2)R-pp binding involves the relea

290 trast, ERK1/2 activation in cells expressing beta-arrestin 2 was predominantly EGF receptor-independe

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

292 onsistent with EMT; beta-arrestin-1, but not beta-arrestin-2, was required for these changes.

293 ernalization of receptors and recruitment of beta-arrestin 2 were unaffected by the loss of 187 glyco

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

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

296 was significantly inhibited by knockdown of beta-arrestin 2 with siRNA in cytokine-treated HLMVECs o

297 horylation of Smo by GRK2 and interaction of beta-arrestin 2 with Smo.

298 , because it is reduced both by depletion of beta-arrestin-2 with small interfering RNA and by elimin

299 phosphorylation confers DOR selectivity for beta-arrestin 2 without affecting the stability of the r

300 sonance energy transfer between CFP-iNOS and beta-arrestin 2-YFP (but not beta-arrestin 1-YFP) that i