ライフサイエンスコーパス: beta-arrestin 1

1 or kinases (GRKs) 2, 3, 5, and 6, as well as beta-arrestin 1.

2 n the Arg(363)-Arg(393) region in the bovine beta-arrestin 1.

3 eceptor selectivity for beta-arrestin 2 over beta-arrestin 1.

4 rectal cancer cells expressing WT and mutant beta-arrestin 1.

5 ansfection with the scaffold/adapter protein beta-arrestin 1.

6 appaB, IkappaBalpha, as a binding partner of beta-arrestin 1.

7 Gbetagamma and c-Src, and possibly involves beta-arrestin 1.

8 ctivation was enhanced by over-expression of beta-arrestin 1.

9 a-arrestin 2 to be 100-fold more potent than beta-arrestin 1.

10 cadaverine, a mutant dynamin I, and a mutant beta-arrestin 1.

11 llowing the overexpression of either GRK2 or beta-arrestin 1.

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

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

14 as being critical to nuclear localization of beta-arrestin-1.

15 e rescued by ectopic expression of wild-type beta-arrestin-1.

16 esponding to the antibody-binding epitope on beta-arrestin-1.

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

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

19 rt, caused by activatory signals mediated by beta-arrestin-1.

20 licated in maintaining the inactive state of beta-arrestin-1.

21 o functionally and conformationally activate beta-arrestin-1.

22 gnizes the phosphopeptide-activated state of beta-arrestin-1.

23 by LC tandem MS, 71 proteins interacted with beta-arrestin 1, 164 interacted with beta-arrestin 2, an

24 oprecipitation of the PAFR and clathrin with beta-arrestin-1, 2) fluorescent resonance energy transfe

25 In contrast, beta-arrestin 1/2 double knockout cells showed greatly e

26 type, beta-arrestin 1, beta-arrestin 2, and beta-arrestin 1/2 knock-out mice.

27 could indeed be detected in IL-8-stimulated beta-arrestin 1/2 knockout cells, and cytoplasmic Rac wa

28 FLAG epitope-tagged beta-arrestin 2 into the beta-arrestin 1/2 null background restored EGF receptor-

29 ed transcriptional responses observed in the beta-arrestin 1/2 null background were lost.

30 In the beta-arrestin 1/2 null background, 1 h of exposure to LP

31 acid did not stimulate TGR5 association with beta-arrestin 1/2 or G protein-coupled receptor kinase (

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

33 al-regulated kinase 1 and 2 phosphorylation, beta-arrestin 1/2 recruitment, and MOP trafficking, and

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

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

36 iants affected in both cAMP accumulation and beta-arrestin-1/2 recruitment.

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

38 minant-negative form of the beta-arrestin 1, beta-arrestin 1 (319-418), blocked agonist-mediated inte

39 ulated inositol phosphate production by 48% (beta-arrestin-1), 71% (beta-arrestin-2), and 84% (beta-a

40 both G-protein-coupled receptor-kinase 2 and beta-arrestin-1, a G-protein-coupled receptor adaptor pr

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

42 We found that beta-arrestin 1 acted as a scaffold for PHLPP2 and Akt1,

43 and completely reversed PAR(2), Galphaq, and beta-arrestin-1 activation in early endosomes and ERK ac

44 carcinoma cells, the increased expression of beta-arrestin-1 after glucocorticoid treatment impairs G

45 ated that Galpha(i), betagamma subunits, and beta-arrestin-1 all play a critical role in IGF-I mitoge

46 Here we report the crystal structure of beta-arrestin-1 (also called arrestin-2) in complex with

47 oexpressed isoforms of beta-arrestin (termed beta arrestin 1 and 2) are highly similar in amino acid

48 -2 and show, in vitro, that these domains in beta-arrestin 1 and 2 interact equally well with AP-2 in

49 Both beta-arrestin 1 and 2 interact with IkappaBalpha in tran

50 Besides their role in desensitization, beta-arrestin 1 and 2 promote the formation of signaling

51 incubated with progastrin or Bmp2; levels of beta-arrestin 1 and 2 were knocked down using small inte

52 Recently, however, beta-arrestin 1 and 2 were shown to activate two downstr

53 To better define differences in the roles of beta-arrestin 1 and 2, we prepared mouse embryonic fibro

54 mice and cultured human cells via CCK2R- and beta-arrestin 1 and 2-dependent suppression of Bmp2 sign

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

56 hway that required CCK2R and was mediated by beta-arrestin 1 and 2.

57 activate RhoA, the concurrent recruitment of beta-arrestin 1 and activation of G(alphaq/11) leads to

58 f PD, and reciprocally affects expression of beta-arrestin 1 and beta-arrestin 2 in microglia in PD m

59 raction of the phosphorylated receptors with beta-arrestin 1 and beta-arrestin 2.

60 alling complex was made by docking activated beta-arrestin 1 and beta2AR crystal structures into the

61 The interaction of beta-arrestin 1 and c-Src is critical for the regulation

62 The former defect was attributed to enhanced beta-arrestin 1 and phosphodiesterase 4 activities, whil

63 /11) in response to ET-1 stimulation, and 2) beta-arrestin 1 and Src kinase form a molecular complex

64 onse involved formation of a complex between beta-arrestin 1 and the Akt phosphatase PHLPP2, and acti

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

66 beta-Arrestin-1 and -2 can mediate activatory signals by

67 and 3) rapid and transient redistribution of beta-arrestin-1 and -2 from the cytosol to the plasma me

68 immunoreactive Galphaq/11, GRK-2 and -3, and beta-arrestin-1 and -2 in a subpopulation of neurons.

69 tion of NK1-R, Galphaq/11, GRK-2 and -3, and beta-arrestin-1 and -2 in cultured myenteric neurons.

70 ne, followed by a striking redistribution of beta-arrestin-1 and -2 to endosomes containing the NK1-R

71 TSH stimulated translocation of beta-arrestin-1 and -2 to TSHR, whereas C2 failed to tra

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

73 ons that may be mediated by GRK-2 and -3 and beta-arrestin-1 and -2.

74 erize the cellular localization of wild type beta-arrestin-1 and a series of N domain mutants to dete

75 that glucocorticoids differentially regulate beta-arrestin-1 and beta-arrestin-2 gene expression in m

76 Alterations in the cellular complement of beta-arrestin-1 and beta-arrestin-2 occur in many human

77 luding stimulation of Ca(2)(+) mobilization, beta-arrestin-1 and beta-arrestin-2 recruitment, and ext

78 The nonvisual arrestins, beta-arrestin-1 and beta-arrestin-2, are multifunctional

79 dicated that E2 increased the recruitment of beta-arrestin-1 and c-Src to ERalpha.

80 Furthermore, there was significantly more beta-arrestin-1 and E2F1 associated with these promoters

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

82 mulation to ERK activation and lipolysis; 3) beta-arrestin-1 and G alpha(q/11) can mediate TNFalpha-i

83 uitin content of IRS-1, suggesting that both beta-arrestin-1 and IRS-1 competitively bind to Mdm2.

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

85 -arrestin-1 content due to ubiquitination of beta-arrestin-1 and proteosome-mediated degradation.

86 gation requires CME and causes engagement of beta-arrestin-1 and recruitment of a p38 MAPK signalosom

87 oid receptor (GR) to induce the synthesis of beta-arrestin-1 and repress the expression of beta-arres

88 can be enhanced by the presence of GRK2 and beta-arrestin-1 and show that these molecules have multi

89 ons, and normalized expression of glomerular beta-arrestin-1 and Snail.

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

91 H receptors in fibroblasts from mice lacking beta-arrestin-1 and/or beta-arrestin-2.

92 beta-arrestins (1 and 2) are widely expressed cytosolic

93 beta-Arrestins 1 and 2 are multifunctional adaptor prote

94 ciprocal effects of down-regulated levels of beta-arrestins 1 and 2 are primarily due to differences

95 Upon their discovery, beta-arrestins 1 and 2 were named for their capacity to

96 Coexpression of beta-arrestins 1 and 2, regulators of G-protein signalin

97 functional adaptor and transducer molecules, beta-arrestins 1 and 2.

98 ctive than palmitate or oleate in recruiting beta-arrestins 1 and 2.

99 arrestin-1), 71% (beta-arrestin-2), and 84% (beta-arrestins-1 and -2).

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

101 uitination of TRPV4, a process that requires beta-arrestin 1, and subsequently to internalization and

102 ansfer-positive interactions among the PAFR, beta-arrestin-1, and clathrin, 3) recruitment and activa

103 eptor (IGF-IR) endocytosis is facilitated by beta-arrestin-1, and internalization is necessary for IG

104 yclase signaling, to a strong recruitment of beta-arrestin-1, and to a positive cross talk of D1R and

105 Microinjection of beta-arrestin 1 antibody inhibited ET-1- but not insulin

106 Microinjection of anti-beta-arrestin-1 antibody specifically inhibited IGF-I mi

107 2 on beta-arrestin and the amino terminus of beta-arrestin-1 are required for this effect of beta-arr

108 In mice and in human cell lines, beta-arrestin-1 (ARRB1), activated via beta(2)-adrenorec

109 ve state of visual arrestin (arrestin 1) and beta-arrestin 1 (arrestin 2) have been resolved.

110 re, our data implicate a functional role for beta-arrestin 1 as a mediator of cellular migration and

111 R signaling, and highlight the importance of beta-arrestin-1 as a target molecule for this desensitiz

112 munoprecipitation experiments, we found that beta-arrestin 1 associated with the ETA receptor in an a

113 hosphorylation coincided with an increase in beta-arrestin 1-associated PGES3 and an arrestin-depende

114 p85 within the pseudopodia, suggesting that beta-arrestin-1 association with PI3K may spatially rest

115 This was associated with a decrease in beta-arrestin-1 association with the beta2-AR as well as

116 eumococci-induced colocalization of PAFr and beta-arrestin 1 at the plasma membrane of endothelial ce

117 Arenas et al (2014) describe a novel role of beta-arrestin-1 at the IS periphery: endocytosis of TCRs

118 generated different fragmentation of bovine beta-arrestin 1, at Pro(276).

119 Overexpression of wild-type (WT) beta-arrestin-1 attenuated insulin-induced degradation o

120 Here, we report that beta-arrestin-1 (barr1), an intracellular protein known

121 ryonic fibroblast (MEF) cells lacking either beta-arrestin 1 (beta arr1(-/-)) or beta-arrestin 2 (bet

122 ac macromolecular complex involving VDCC and beta-arrestin 1 (beta-Arr1) into clathrin-coated vesicle

123 a novel bypass mechanism through which ETAR/beta-arrestin-1 (beta-arr1, ARRB1) links Wnt signaling t

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

125 However, a dominant-negative form of the beta-arrestin 1, beta-arrestin 1 (319-418), blocked agon

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

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

128 ing fibroblast lines derived from wild type, beta-arrestin 1, beta-arrestin 2, and beta-arrestin 1/2

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

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

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

132 Co-expression of PAR1 with beta-arrestin 1 (betaarr1) in COS-7 cells resulted in a

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

134 We investigated whether adrenal beta-arrestin 1 (betaarr1)-mediated aldosterone producti

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

136 beta-Arrestin-1 (betaArr1) plays a major role in the des

137 beta-Arrestin-1 (betaArr1), a scaffolding protein critic

138 dependent aldosterone production mediated by beta-arrestin-1 (betaarr1), a universal heptahelical rec

139 we show that in NCM460 cells exposed to NT, beta-arrestin-1 (betaARR1), and beta-arrestin-2 (betaARR

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

141 and the allosteric modulation of ACKR3 upon beta-arrestin 1 binding.

142 ion of the LH/CG R, and that the trigger for beta-arrestin-1 binding to the LH/CG R appears to be R a

143 ASK1/p38 MAPK heterodimer is recruited to a beta-arrestin-1 bound MKK3.

144 t receptor exhibits reduced association with beta-arrestin 1 but continues to exhibit association wit

145 A mutants of CXCR2 exhibit normal binding to beta-arrestin 1 but exhibit decreased binding to adaptin

146 Conversely, suppression of beta-arrestin 1, but not beta-arrestin 2, expression by

147 ablate tight junctions consistent with EMT; beta-arrestin-1, but not beta-arrestin-2, was required f

148 by depletion of cellular beta-arrestin 2 and beta-arrestin 1 by small interfering RNA.

149 Down-regulation of beta-arrestin-1 by siRNA inhibited TSH-stimulated phosph

150 Edman degradation analysis of a beta-arrestin 1 C-terminal fragment fused to enhanced gr

151 These results show that the prostaglandin E/beta-arrestin 1/c-Src signaling complex is a crucial ste

152 association of a prostaglandin E receptor 4/beta-arrestin 1/c-Src signaling complex resulting in the

153 a clearly show that both visual arrestin and beta-arrestin 1 can bind to monomeric rhodopsin and stab

154 In summary, we have found the following: (i) beta-arrestin-1 can alter insulin signaling by inhibitin

155 molecules in the TNFalpha action cascade; 2) beta-arrestin-1 can couple TNFalpha stimulation to ERK a

156 beta-arrestin-dependent mechanism, and that beta-arrestin-1 can directly associate with and inhibit

157 ponent G alpha(q/11) and the adapter protein beta-arrestin-1 can function as signaling molecules in t

158 vity blocks PAR-2-stimulated chemotaxis, and beta-arrestin-1 colocalizes with p85 within the pseudopo

159 x shows marked conformational differences in beta-arrestin-1 compared to its inactive conformation.

160 ing and purifying a functional human beta2AR-beta-arrestin-1 complex that allowed us to visualize its

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

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

163 es an approximately 50% decrease in cellular beta-arrestin-1 content due to ubiquitination of beta-ar

164 This insulin-induced decrease in beta-arrestin-1 content was blocked by inhibition of pho

165 the transducer-free, Gq-protein-coupled, and beta-arrestin-1-coupled states.

166 duced proteasomal degradation of IRS-1; (ii) beta-arrestin-1 decreases the rate of ubiquitination of

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

168 n and enhanced IL-10 and IL-22 production in beta-arrestin-1-deficient mice likely lead to attenuated

169 Chronic insulin treatment leads to enhanced beta-arrestin-1 degradation.

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

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

172 inositol phosphate signaling while enhancing beta-arrestin-1-dependent stimulation of the MAPK pathwa

173 Cotransfection with beta-arrestin 1 did not increase the rate or extent of a

174 In insulin-treated, beta-arrestin-1-downregulated cells, there was complete

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

176 Exogenous expression of wild type beta-arrestin-1 enhanced the transcriptional activity of

177 lays important roles in the nucleus, but how beta-arrestin-1 enters the nucleus remains unclear becau

178 podocytes and hyperplastic lesion formation; beta-arrestin-1 expression increased in visceral podocyt

179 igration via ET(A)R activation and increased beta-arrestin-1 expression.

180 lasma membrane that also contained Rab5a and beta-arrestin 1, followed by rapid recycling of the NK1R

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

182 rticoid response elements in intron-1 of the beta-arrestin-1 gene and intron-11 of the beta-arrestin-

183 in insulin-treated cells in which endogenous beta-arrestin-1 had been downregulated rescued IGF-I- an

184 restin 2 is more robust than by active-state beta-arrestin 1, highlighting differential capacities of

185 physical association between the GLP-1 R and beta-arrestin-1 in cultured INS-1 pancreatic beta cells.

186 sustained activation of PAR(2), Galphaq, and beta-arrestin-1 in early endosomes and activated extrace

187 Our goal was to investigate the role of beta-arrestin-1 in IBD using mouse models of colitis.

188 els, have demonstrated an important role for beta-arrestin-1 in inflammation.

189 Ectopic expression of wild-type beta-arrestin-1 in insulin-treated cells in which endoge

190 oimmunoprecipitated with follicular membrane beta-arrestin-1 in response to LH/CG R activation compar

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

192 However, the role of beta-arrestin-1 in the pathogenesis of inflammatory bowe

193 Neutralization of beta-arrestin-1 inhibited all of these cellular events,

194 Knockdown of beta-arrestin-1 inhibited TSH-stimulated up-regulation o

195 btypes differentially regulate ASM GPCRs and beta-arrestin-1 inhibition represents a novel approach t

196 Small interfering RNA-mediated knockdown of beta-arrestin-1 inhibits TNFalpha-induced tyrosine phosp

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

198 beta-Arrestin 1 interacts with, and acts as an adaptor f

199 beta-Arrestin 1 is required for internalization and mito

200 We now show that beta-arrestin 1 is required to activate the small GTPase

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

202 beta-arrestin-1 is an adaptor protein that mediates agon

203 (ii) This downregulation of endogenous beta-arrestin-1 is associated with decreased IGF-I-, LPA

204 We found that beta-arrestin-1 is associated with TRAF2 (TNF receptor-a

205 In the present study, we determined whether beta-arrestin-1 is involved in insulin-induced insulin r

206 we demonstrate that the scaffolding protein beta-arrestin-1 is necessary for nicotine-mediated induc

207 work, we found that beta-arrestin 2, but not beta-arrestin 1, is required for LPA-induced NF-kappaB a

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

209 imulates lipolysis in 3T3-L1 adipocytes, and beta-arrestin-1 knockdown blocks the effects of TNFalpha

210 beta-Arrestin-1 knockdown broadly attenuated GLP-1 signa

211 However, beta-arrestin-1 knockdown did not affect GLP-1 R surface

212 rotein-1 and matrix metalloproteinase 3, and beta-arrestin-1 knockdown inhibited both of these effect

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

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

215 To this end, we subjected wild-type (WT) and beta-arrestin-1 knockout (beta-arr-1(-/-)) mice to colit

216 on IRS-1 degradation; and (iv) inhibition of beta-arrestin-1 leads to enhanced IRS-1 degradation and

217 ic insulin treatment down-regulates cellular beta-arrestin 1 levels, leading to a marked impairment i

218 h these promoters in human NSCLC tumors, and beta-arrestin-1 levels correlated with vimentin and fibr

219 Increased beta-arrestin-1 levels in podocytes retrieved from cresc

220 Recent evidence indicates that beta-arrestin 1 may act as an important mediator in G pr

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

222 Arg323 and Lys409 residues were required for beta-arrestin-1-mediated sustained ERK phosphorylation a

223 th phosphoinositide (PI) hydrolysis and with beta-arrestin-1-mediated sustained extracellular signal-

224 -induced signaling mechanism for CB1 wherein beta-arrestin 1 mediates short term signaling to ERK1/2

225 beta-Arrestin-1 mediates agonist-dependent desensitizati

226 -1 action, showing that the scaffold protein beta-arrestin-1 mediates the effects of GLP-1 to stimula

227 Addition of recombinant purified beta-arrestin-1 mimicked human chorionic gonadotrophin t

228 e of Cell, Kang et al. provide evidence that beta-arrestin 1 moves to the nucleus in response to GPCR

229 Expression of a phosphorylation-independent beta-arrestin 1 mutant (R169E) significantly rescued the

230 We also show a beta-arrestin 1 mutant, which engages coated structures

231 beta-Arrestin 1 mutants, impaired either in c-Src bindin

232 Whereas neither beta-arrestin 1 nor G(alphaq/11) activation alone is suf

233 hese results demonstrate a critical role for beta-arrestin-1 nuclear localization in scaffolding and

234 Mutation of the NLS led to a loss of beta-arrestin-1 nuclear localization in transfected cell

235 Loss of beta-arrestin-1 nuclear localization was accompanied by

236 uctural basis and functional implications of beta-arrestin-1 nuclear localization.

237 Second, overexpression of arrestin 2 or 3 (beta-arrestin 1 or 2) abolished the V2 receptor-mediated

238 g to other G proteins (G(s), G(12), G(o)) or beta-arrestin 1 or 2.

239 beta-Arrestin 1 or beta-arrestin 2 depletion prevented t

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

241 Overexpression of either beta-arrestin 1 or beta-arrestin 2 led to marked inhibit

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

243 gnals via beta-arrestin, and in mice lacking beta-arrestin-1 or -2, KP-triggered GnRH secretion is si

244 inin B2 receptor (B2R) complexes with either beta-arrestin-1 or -2.

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

246 In select experiments, beta-arrestin-1 or dynamin-2 were neutralized by intrace

247 DNA constructs that encode dominant negative beta-arrestin-1 or dynamin.

248 ing RNA approach for selectively suppressing beta-arrestins 1 or 2 expression by up to 95%.

249 However, upon coexpression of arrestin-2 (beta-arrestin-1) or arrestin-3 (beta-arrestin-2), intern

250 These results suggest that endogenous beta-arrestin-1 participates in agonist-dependent desens

251 in membrane-associated beta-arrestin-1, that beta-arrestin-1 participates in agonist-dependent desens

252 rat beta-arrestin-2 (PET(178)P), but not rat beta-arrestin-1 (PER(177)P).

253 a(i)-associated pathway; and (iii) increased beta-arrestin 1 phosphorylation at Ser-412.

254 Taken together, these studies indicate that beta-arrestin-1 plays a role in GLP-1 signaling leading

255 A mounting body of evidence suggests that beta-arrestin-1 plays important roles in the nucleus, bu

256 Silencing of beta-arrestin-1 prevented podocyte phenotypic changes an

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

258 G protein-coupled receptor kinase 3 (GRK3), beta-arrestin-1, Pyk2, and focal adhesion kinase (FAK).

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

260 ptor in an agonist-dependent manner and that beta-arrestin 1 recruited Src kinase to a molecular comp

261 hermore, D1R or D3R antagonists counteracted beta-arrestin-1 recruitment and MAPK activation induced

262 We conclude that PAF signaling requires CME, beta-arrestin-1 recruitment of a p38 MAPK signalosome, a

263 xpression of a dominant negative fragment of beta-arrestin-1 reduces PAR-2-stimulated internalization

264 beta-Arrestin 1 selectively binds to the SNARE-binding r

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

266 Whether beta-arrestin 1 serves a functional role in these events

267 A549-luciferase cells lacking beta-arrestin-1 showed a significantly reduced capacity

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

269 In contrast, beta-arrestin 1 siRNA had no effect.

270 Transfection of neurons with beta-arrestin-1 small interfering RNA prevented E2-induc

271 restin-1 was knocked down by transfection of beta-arrestin-1 small interfering RNA, insulin-induced I

272 n with the beta2-AR as well as a decrease in beta-arrestin-1-Src and Src-beta2-AR association.

273 rough mGlu1a receptors require expression of beta-arrestin-1, suggesting a possible role for receptor

274 Finally, GRK2 and beta-arrestin-1 synergistically enhanced both the rate a

275 atterns induce distinct structural states of beta-arrestin-1 that are coupled to distinct arrestin fu

276 varian follicles contain membrane-associated beta-arrestin-1, that beta-arrestin-1 participates in ag

277 onship of small ligands, the binding mode of beta-arrestin 1, the activation dynamics, and the atypic

278 follicular membranes unexpectedly contained beta-arrestin-1, the role of arrestins in desensitizatio

279 ategy to retrieve AT(1)R-engaged isoforms of beta-arrestin 1 to confirm direct interaction of fragmen

280 10 nM) induced translocation of the NK1R and beta-arrestin 1 to perinuclear sorting endosomes contain

281 al reconstructions reveal bimodal binding of beta-arrestin 1 to the beta2AR, involving two separate s

282 iotensin stimulation leads to recruitment of beta-arrestin 1 to this complex.

283 Activated ET(A)R recruited beta-arrestin-1 to form a trimeric complex with Src lead

284 protein-coupled receptor kinase-2 (GRK2) and beta-arrestin-1 to regulate the phosphorylation state an

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

286 tion of CB1-GFP with red fluorescent protein-beta-arrestin 1 upon ORG27569 treatment using confocal m

287 cterize the interactions between beta2AR and beta-arrestin 1 using hydrogen-deuterium exchange mass s

288 The structure of the beta-arrestin-1-V2Rpp-Fab30 complex shows marked conform

289 The overexpression of either the beta-arrestin 1-V53D dominant negative inhibitor of beta

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

291 beta-Arrestin-1 was associated with the receptors for IG

292 When endogenous beta-arrestin-1 was knocked down by transfection of beta

293 ased dynamics in both the N and C domains of beta-arrestin 1 when coupled to the beta2AR.

294 ynergistically enhanced by cotransfection of beta-arrestin-1, which had no effect on m2 mAChR functio

295 iation was inhibited to overexpression of WT beta-arrestin-1, which led by decreased ubiquitin conten

296 ues suggest engagement of the finger loop of beta-arrestin 1 with the seven-transmembrane core of the

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

298 ound a marked decrease in the association of beta-arrestin-1 with the IGF-IR and a 55% inhibition of

299 Interaction of beta-arrestin-1 with the muOR core binding site appears

300 en CFP-iNOS and beta-arrestin 2-YFP (but not beta-arrestin 1-YFP) that increased 3-fold after B1R sti