ライフサイエンスコーパス: arrestin

1 smembrane segments 1 and 4 and the C-lobe of arrestin.

2 ability to signal via either Galphas or beta-arrestin.

3 r regulating receptor interactions with beta-arrestin.

4 iary signaling protein, such as G protein or arrestin.

5 elective activation of G protein versus beta-arrestin.

6 phas, while Src activation depends solely on arrestin.

7 ling, with no measurable recruitment of beta-arrestin.

8 ver, CysLTR2-L129Q only poorly recruits beta-arrestin.

9 PSMalpha2 in promoting FPR2 to recruit beta-arrestin.

10 ensitive G protein but did not activate beta-arrestin.

11 am cellular responses via G proteins or beta-arrestin.

12 s' that influence the global conformation of arrestin.

13 ctionally relevant conformational changes of arrestin.

14 edicted to affect its interactions with beta-arrestin.

15 ent pathways mediated by G proteins and beta-arrestins.

16 vate pathways mediated by G proteins or beta-arrestins.

17 upled receptors signal through G proteins or arrestins.

18 esses via heterotrimeric G proteins and beta-arrestins.

19 inked G-proteins and the recruitment of beta-arrestins.

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

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

22 GPCR kinases (GRKs) and by coupling of beta-arrestin 1 (betaarr1, also known as arrestin 2), which d

23 keletal muscle hypertrophy were lost in beta-arrestin 1 knockout mice, implying that arrestins, multi

24 e A inhibition by H-89 and knockdown of beta-arrestin 1 or beta-arrestin 2 did not affect the decreas

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

26 skeletal muscle and this is mediated by beta-arrestin 1.

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

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

29 proteins and investigate how the binding of arrestin-1 affects the catalytic activity of enolase-1.

30 Beta-arrestin-1 and -2 (Barr1 and Barr2, respectively) are in

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

32 assays in A549 cells, we observed that beta-arrestin-1 and unliganded GR interact in the cytoplasm a

33 dy, we investigated one of these alternative arrestin-1 binding partners, the glycolysis enzyme enola

34 these peptides modulate the conformation of arrestin-1 by nuclear magnetic resonance (NMR).

35 selective substitution of two amino acids in arrestin-1 can completely remove its effect on enolase-1

36 Compared with a structure of a rhodopsin-arrestin-1 complex, in our structure arrestin is rotated

37 size of the oligomers is not the reason for arrestin-1 exclusion from the outer segments in the dark

38 eptor survival.SIGNIFICANCE STATEMENT Visual arrestin-1 forms dimers and tetramers.

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

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

41 Arrestin-1 is also well-known to interact with additiona

42 Like wild type, mutant arrestin-1 is largely excluded from the outer segments i

43 d type, demonstrating that in vivo monomeric arrestin-1 is necessary and sufficient for this function

44 Arrestin-1 is the arrestin family member responsible for

45 xpressed oligomerization-deficient mutant in arrestin-1 knock-out mice.

46 oligomerization reduces the cytotoxicity of arrestin-1 monomer, ensuring long-term photoreceptor sur

47 n reduces the cytotoxicity of high levels of arrestin-1 monomer.

48 In rods, arrestin-1 moves from the inner segments and cell bodies

49 To determine the biological role of visual arrestin-1 oligomerization in rod photoreceptors, we exp

50 ocalization is not due the size exclusion of arrestin-1 oligomers.

51 ties for examining the functional effects of arrestin-1 on enolase-1 activity in photoreceptors and t

52 on the arrestin-1 surface, we observed that arrestin-1 primarily engages enolase-1 along a surface t

53 High expression of oligomerization-deficient arrestin-1 resulted in rod death.

54 To test the role of arrestin-1 self-association, we expressed oligomerizatio

55 of strategically placed fluorophores on the arrestin-1 surface, we observed that arrestin-1 primaril

56 ng a surface that is opposite of the side of arrestin-1 that binds photoactivated rhodopsin.

57 n in rod photoreceptors, we expressed mutant arrestin-1 with severely impaired self-association in mo

58 of a phospho-beta2 adrenergic receptor/beta-arrestin-1(beta-arr1) membrane protein signaling complex

59 between the glucocorticoid receptor and beta-arrestin-1, a scaffold protein with a well-established r

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

61 ly internalized on codeine binding in a beta-arrestin-1-dependent manner.

62 ation, we developed a molecular model of the arrestin-1-enolase-1 complex, which was validated by tar

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

64 n of ERK1/2 in cells that are devoid of beta-arrestin-1/2.

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

66 IFN signaling remained intact, despite beta-arrestin 2 activation, as IFN-beta, IFN-gamma, IFN-lambd

67 We showed that CCL5 recruits both arrestin 2 and arrestin 3 to CCR5 with recruitment, part

68 We identify beta-arrestin 2 as a key modulator of type I IFN in primary h

69 Small interfering RNA knockdown of beta-arrestin 2 demonstrated its role in IFNAR1 internalizati

70 -89 and knockdown of beta-arrestin 1 or beta-arrestin 2 did not affect the decreased cAMP production

71 tion of the receptor and recruitment of beta-arrestin 2 in human embryonic kidney cell line 293 cells

72 on of a dominant negative dynamin 1 and beta-arrestin 2 knockdown had no effect, we concluded that do

73 beta-Arrestin 2 was selectively activated by CCL2/CCR2 signal

74 ited improved functional potency (cAMP, beta-arrestin 2), metabolic stability, and aqueous solubility

75 of beta-arrestin 1 (betaarr1, also known as arrestin 2), which displaces G(s) and induces signalling

76 3 to CCR5 with recruitment, particularly of arrestin 2, strongly dependent on the arrestin tail inte

77 gnaling through ligand-independent, but beta-arrestin 2-dependent mechanisms.

78 showed isoform bias toward arrestin 3 versus arrestin 2.

79 ort the novel finding that mice lacking beta-arrestin-2 (barr2) selectively in adipocytes show signif

80 ational equilibrium of the highly homologous arrestin-2 and arrestin-3 and found that these two isofo

81 y vertebrates have two non-visual arrestins, arrestin-2 and arrestin-3.

82 agonists biased against recruitment of beta-arrestin-2 could provide analgesic efficacy with fewer s

83 In the presence of IP(6), arrestin-2 forms "infinite" chains, where each promoter

84 n of eight residues that is conserved across arrestin-2 homologs, but absent in arrestin-3 that likel

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

86 contrast, ECD-scFvhFc potently inhibits beta-arrestin-2 recruitment after PTH (1-34)-driven receptor

87 ERK1/2 phosphorylation, in addition to beta-arrestin-2 recruitment and downstream arrestin-dependent

88 hosphorylation of FFA4-L and subsequent beta-arrestin-2 recruitment and extracellular-signal regulate

89 ), while they only show weak or even no beta-arrestin-2 recruitment at both beta(1)- and beta(2)-AR.

90 q) protein activation and in particular beta-arrestin-2 recruitment at OX1R.

91 -associated effects on thrombin-induced beta-arrestin-2 recruitment to and signaling of PAR1 could be

92 uced the efficacy of thrombin to induce beta-arrestin-2 recruitment to recombinant PAR1 and enhanced

93 e for recruitment and interactions with beta-arrestin-2.

94 gical consequences, including differences in arrestin-2/3 trafficking and JNK3 activation.

95 howed that CCL5 recruits both arrestin 2 and arrestin 3 to CCR5 with recruitment, particularly of arr

96 used, recruitment showed isoform bias toward arrestin 3 versus arrestin 2.

97 howed previously that trimeric state induces arrestin-3 activation (Chen et al., 2017).

98 rium of the highly homologous arrestin-2 and arrestin-3 and found that these two isoforms are regulat

99 We previously showed that arrestin-3 can be activated by inositol-hexakisphosphate

100 We found that arrestin-3 exhibited >15-fold higher affinity for inacti

101 In contrast, full length and truncated arrestin-3 form trimers and higher-order oligomers in th

102 eptor-binding surface of arrestin-3, induces arrestin-3 oligomerization, and this oligomer stabilizes

103 uld further help decipher D2R ligand-induced arrestin-3 recruitment and trafficking, with potentially

104 ed across arrestin-2 homologs, but absent in arrestin-3 that likely accounts for the differences in t

105 Here, we used arrestin-3, a scaffold of the ASK1-MKK4/7-JNK3 cascade,

106 teracts with the receptor-binding surface of arrestin-3, induces arrestin-3 oligomerization, and this

107 igomer stabilizes the active conformation of arrestin-3.

108 ave two non-visual arrestins, arrestin-2 and arrestin-3.

109 beta-Arrestin, a molecular sensor of activated GPCRs, and the

110 dings indicate that NTSR1 G protein and beta-arrestin activation produce discrete and separable physi

111 Codeine-triggered beta-arrestin activation was also established by the Tango as

112 ein signaling, but they can also induce beta-arrestin activation, leading to such side effects as res

113 or directing the binding of G protein versus arrestin and for selecting between the activation of ERK

114 the phosphorylation pattern influences both arrestin and Galphas coupling, suggesting an additional

115 e found that ERK1/2 activation involves both arrestin and Galphas, while Src activation depends solel

116 peptides lacked the ability to recruit beta-arrestin and induce neutrophil chemotaxis, supporting th

117 tein signaling to a greater extent than beta-arrestin and internalization signaling pathways.

118 s, but the functional interplay between beta-arrestin and the BBSome remains elusive.

119 large bias factors toward G protein or beta arrestin are required for investigating the translationa

120 argets in the treatment of dementia, and the arrestins are common to their signaling.

121 rential engagement of G proteins versus beta-arrestins are commonly limited by the small response win

122 Cellular functions of arrestins are determined in part by the pattern of phosp

123 unctional differences between two non-visual arrestins are in part determined by distinct modes of th

124 beta-Arrestins are major regulators of G protein-coupled rece

125 eins that block receptor-G protein coupling, arrestins are now appreciated for their expanding repert

126 The arrestins are ubiquitously expressed adaptor proteins th

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

128 aling 2, RGS2; GPCR Kinase 5, GRK5; and beta-arrestin, Arrb2) using RT-PCR, qPCR, and western blot an

129 field is why vertebrates have two non-visual arrestins, arrestin-2 and arrestin-3.

130 s in GPCR internalization and implicate beta-arrestin as a potential player mediating behavioral resp

131 Here, using a fluorescent arrestin assay, we confirmed that the common fungal airw

132 chemokine in the extent and quality of CCR5-arrestin association that they elicit, providing valuabl

133 ion of ACE2, agonism of MAS1 receptors, beta-arrestin-based Angiotensin receptor agonists, and admini

134 etermine how GPCR phosphorylation influences arrestin behavior by using atomic-level simulations and

135 ne and are subsequently desensitized by beta-arrestin (beta-arr).

136 oupled receptor (GPCR) family and binds beta-arrestins (beta-arrs), which regulate AT1R signaling and

137 e signaling cascades via G-proteins and beta-arrestins (betaarr).

138 ding to multifunctional proteins called beta-arrestins (betaarrs).

139 ecular dynamics simulations to determine how arrestin bias and G protein bias arise at the angiotensi

140 iased agonist but also extends profound beta-arrestin bias to the endogenous ligand by selectively an

141 ons to determine how fentanyl, a potent beta-arrestin biased agonist, binds the mu-opioid receptor (m

142 olecular insight into fentanyl mediated beta-arrestin biased signaling and a rational framework for f

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

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

145 cs simulations of bilorphin and the strongly arrestin-biased endomorphin-2 with the MOPr indicate dis

146 s been suggested to be an intrinsically beta-arrestin-biased GPCR.

147 has been demonstrated to function as a beta-arrestin-biased ligand for the beta(2)AR, stimulating be

148 ystal structures of HTR2A complexed with the arrestin-biased ligand LSD or the inverse agonist methio

149 Harnessing beta-arrestin-biased MC4R signaling may represent an effectiv

150 s issue of Cell, Slosky et al. report a beta-arrestin-biased neurotensin receptor ligand that may cur

151 ell surface activates cancer-protective beta-arrestin-biased signaling (beta-arr-BS).

152 oid peptides that efficaciously recruit beta-arrestin, bilorphin is G protein biased, weakly phosphor

153 G protein-coupled receptors (GPCRs) to which arrestins bind.

154 sphorylation sites: 'key sites' required for arrestin binding and activation, an 'inhibitory site' th

155 l the effects of phosphorylation patterns on arrestin binding and conformation.

156 s (GPCRs) by GPCR kinases (GRKs) facilitates arrestin binding and receptor desensitization.

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

158 d (i.e., C-terminal phosphorylation and beta-arrestin binding), but a detailed analysis of melanopsin

159 ivation, an 'inhibitory site' that abrogates arrestin binding, and 'modulator sites' that influence t

160 Despite high-resolution structural data of arrestins bound to phosphorylated receptor C-termini, th

161 The apo, full agonist-, and arrestin-bound states of Y2R were prepared by cell-free

162 he development of a D2R mutant that recruits arrestin but is devoid of G protein activity.

163 rmations that are capable of activating beta-arrestin but not heterotrimeric G(q) protein signaling.

164 5-HT(2)R endocytic machinery, including beta-arrestin, clathrin, AP2, and dynamin, significantly redu

165 ctivation as well as endosomal receptor-beta-arrestin complex stabilization in the mitogenic response

166 patterns selectively favor a wide variety of arrestin conformations, differently affecting arrestin s

167 contrast, circulatory S1P-dependent S1PR1/B-arrestin coupling was observed in non-branch point aEC2

168 To understand the molecular basis for arrestin coupling, here we determined the cryo-electron

169 id peptide DAMGO require M153 to induce beta-arrestin coupling, while M153 was dispensable for G prot

170 s (aEC1) exhibits ligand-independent S1PR1/B-arrestin coupling.

171 ion, and this ROS response was suppressed by arrestin-dependent activation of the MAPK p38.

172 sing receptor (CaSR) internalization is beta-arrestin-dependent and sensitive to modulation by allost

173 d ligand for the beta(2)AR, stimulating beta-arrestin-dependent but not G protein-dependent signaling

174 s greatly reduced, leading to decreased beta-arrestin-dependent ERK1/2 activation, faster recycling o

175 o beta-arrestin-2 recruitment and downstream arrestin-dependent ERK1/2 phosphorylation and internaliz

176 beta-arrestin-dependent ERK1/2 regulation is the subject of i

177 AT1R by angiotensin II (ANGII) elicits beta-arrestin-dependent inhibition and internalization of TRP

178 imaging, phosphate radiolabeling, and a beta-arrestin-dependent luciferase assay, we characterize a G

179 ns comprising K63 linkages (UbK63) in a beta-arrestin-dependent manner before BBSome-mediated exit.

180 rs cell membrane blebbing in a RhoA-and beta-arrestin-dependent manner.

181 ld enhance skeletal muscle strength via beta-arrestin-dependent pathways.

182 ctates non-GPCR interactions specifying beta-arrestin-dependent signaling by a GPCR.

183 nificantly lower receptor upregulation (beta-Arrestin-dependent signaling pathway) upon stimulation c

184 G protein-dependent as well as non-canonical arrestin-dependent signaling pathways.

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

186 arly in ligand naive cells, yet exhibit beta-arrestin-dependent signaling responses, mitogen-activate

187 To study the link between beta-arrestin-dependent trafficking and ERK1/2 signaling, we

188 g evidence that CaSR internalization is beta-arrestin-dependent while interestingly being largely ind

189 Additionally, beta-arrestin directly regulates many cell signalling pathway

190 hr(349)) located within the C-terminal alpha-arrestin domain and proximal to a previously characteriz

191 Arrestin domain-containing 3 (Arrdc3) is a member of the

192 PCRs and G proteins, less is known about how arrestins engage GPCRs.

193 buse, the effect of alcohol exposure on beta-arrestin expression and beta-arrestin-mediated GPCR traf

194 Arrestin-1 is the arrestin family member responsible for inactivation of t

195 ntaining 3 (Arrdc3) is a member of the alpha-arrestin family previously linked to human obesity.

196 ur AATs during starvation required the alpha-arrestin family protein Art2/Ecm21, an adaptor for the u

197 ons by detecting the binding of G protein or arrestin fragments that have been fused onto the recepto

198 R phosphorylation patterns might control how arrestin functions in the cell.

199 rent "core" and "tail" interaction model for arrestin-GPCR interaction.

200 ocking the recruitment and signaling of beta-arrestin in response to ghrelin.

201 The relative roles of G proteins versus arrestins in initiating and directing signaling is hotly

202 duced ROS generation resulted from the early arrestin-independent phase of JNK activation, and this R

203 ulated biphasic JNK activation with an early arrestin-independent phase, requiring the small G protei

204 mporally correlated with increased GPCR/beta-arrestin interaction signals in response to agonist trea

205 t occur later than agonist-induced GPCR/beta-arrestin interaction signals, indicating that GPCR/14-3-

206 lization and infection, suggesting that beta-arrestin interactions with 5-HT(2A)R are critical for JC

207 1R variants that show distinct receptor-beta-arrestin interactions: A163T, T282M, and C289W.

208 odopsin-arrestin-1 complex, in our structure arrestin is rotated by approximately 85 degrees relative

209 mu-opioid receptor and interaction with beta-arrestins is controlled by carboxyl-terminal phosphoryla

210 that PX exploits the antagonism between beta-arrestin isoforms; in low ligand conditions, PX favored

211 preferentially through either G proteins or arrestins-known as biased agonism(3)-is important in dru

212 Although beta-arrestin levels are influenced by various drugs of abuse

213 2 receptor aggregation was inhibited by beta-arrestin-mediated downregulation.

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

215 t phosphorylation patterns trigger different arrestin-mediated effects.

216 xposure on beta-arrestin expression and beta-arrestin-mediated GPCR trafficking is poorly understood.

217 Thus, TAS2R14 is subject to beta-arrestin-mediated internalization and subsequent down-re

218 and suggest conformationally dependent beta-arrestin-mediated MAPK activation as well as endosomal r

219 fety profiles are due to a reduction in beta-arrestin-mediated signaling or, alternatively, to their

220 beta-arrestin 1 knockout mice, implying that arrestins, multifunctional adapter and signaling protein

221 us, in response to IP(6), the two non-visual arrestins oligomerize in different ways in distinct conf

222 buted to the preferential activation of beta-arrestin over G proteins, make methadone a standard-of-c

223 e effects of MRAP2 on the Galpha(q) and beta-arrestin pathways were independent and involved distinct

224 Arrestin proteins bind to active, phosphorylated G-prote

225 n, a process initiated by the recruitment of arrestin proteins.

226 both conserved aspects and plasticity among arrestin-receptor interactions.

227 The analysis quantified the initial rate of arrestin recruitment (k(tau)), a biologically-meaningful

228 osphorylation, as well as DHA-dependent beta-arrestin recruitment and DHA-dependent extracellular-sig

229 cts of loss of phosphorylation sites on beta-arrestin recruitment and ERK1/2 activation.

230 riants exhibiting signaling bias toward beta-arrestin recruitment and increased mitogen-activated pro

231 and NADPH oxidase activity, yet lack of beta-arrestin recruitment and neutrophil chemoattraction.

232 he late phase generally associated with beta-arrestin recruitment and receptor endocytosis, promoting

233 calmodulin-dependent manner, preventing beta-arrestin recruitment and receptor internalization.

234 ducted a high-throughput screen using a beta-arrestin recruitment assay.

235 ciation kinetic measurements coupled to beta-arrestin recruitment assays to investigate ACKR3:chemoki

236 adioligand binding displacement assays, beta-arrestin recruitment assays, cyclic AMP inhibition assay

237 e of melatonin, 28, had dramatically reduced arrestin recruitment at MT(2), while compound 37 was dev

238 ceptors in close proximity, but impedes beta-arrestin recruitment by all receptors tested.

239 uishable from wild-type D2R, indicating that arrestin recruitment can drive locomotion in the absence

240 changed or exacerbated, indicating that beta-arrestin recruitment does not contribute to the severity

241 xperiments suggest that reduced or abolished arrestin recruitment does not improve therapeutic window

242 tor activation, G protein coupling, and beta-arrestin recruitment for all tested ligands.

243 ere CCR2-selective, 39 and 43 inhibited beta-arrestin recruitment in CCR5 with high potency.

244 t bias toward G protein activation over beta-arrestin recruitment in comparison to quinpirole.

245 t preferentially and potently activated beta-arrestin recruitment in vitro and potently elicited lowe

246 els of receptor phosphorylation to CCL5, but arrestin recruitment is absolutely dependent on the arre

247 Because beta-arrestin recruitment is dependent on receptor phosphoryl

248 Here we describe a platform for measuring arrestin recruitment kinetics to GPCRs using a high quan

249 tein kinase D (PKD) activation, but not beta-arrestin recruitment or PAR(2) endocytosis.

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

251 bled high temporal resolution measurement of arrestin recruitment to the angiotensin AT(1) and vasopr

252 alcium signaling and is more potent for beta-arrestin recruitment triggered greater levels of platele

253 s within other GPCRs similarly impaired beta-arrestin recruitment while maintaining G protein signali

254 CCR5 hyperphosphorylation, driving enhanced arrestin recruitment with lower dependence on the arrest

255 was assessed by comparing k(tau) values for arrestin recruitment with those for Gq signaling via the

256 roperties ([(35)S]GTPgammaS binding and beta-arrestin recruitment) of 22 peptides at each of the thre

257 MP inhibition, Ca(2+) mobilization, and beta-arrestin recruitment) which identified ERK1/2 phosphoryl

258 /11)-coupled calcium-signaling pathway, beta-arrestin recruitment, and mitogen-activated protein kina

259 Despite the lack of beta-arrestin recruitment, the PSMalpha peptides induced an F

260 city to elicit both CCR5 phosphorylation and arrestin recruitment, with reference to the current "cor

261 ists that block CXCL11- and CXCL12-induced B-arrestin recruitment.

262 ion, AT1R receptor phosphorylation, and beta-arrestin recruitment.

263 as enhancers while minimally activating beta-arrestin recruitment.

264 does not elicit receptor phosphorylation or arrestin recruitment.

265 e inhibition, calcium mobilization, and beta-arrestin recruitment.

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

267 naling and away from other pathways, such as arrestin recruitment.

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

269 s or starvation activate complementary alpha-arrestin-Rsp5-complexes to control selective endocytosis

270 Finally, we identified the likely source of arrestin's modulation of enolase-1 catalysis, showing th

271 AC1) and protein kinase C (PKC), and a later arrestin-scaffolded phase, requiring RAC1 and Ras homolo

272 ation of the receptor or recruitment of beta-arrestin scaffolding proteins could preserve the analges

273 ce G protein signaling without inducing beta-arrestin signaling can alleviate pain while reducing sid

274 nuates G protein signaling and augments beta-arrestin signaling downstream of KOR, exhibiting conside

275 rotrimeric G protein signaling, whereas beta-arrestin signaling is considered central to their detrim

276 However, the mechanism for stimulating beta-arrestin signaling is not known, making it difficult to

277 ngages with effector molecules to drive beta-arrestin signaling.

278 g from canonical G(i/o) to noncanonical beta-arrestin signaling.

279 chemical features dictate G protein or beta-arrestin signaling?

280 ysis of amplified (G protein) versus linear (arrestin) signaling mechanisms, and nonequilibrium effec

281 rrestin conformations, differently affecting arrestin sites implicated in scaffolding distinct signal

282 Members of the arrestin superfamily have great propensity of self-assoc

283 n recruitment is absolutely dependent on the arrestin tail interaction, and in one of the cellular ba

284 rly of arrestin 2, strongly dependent on the arrestin tail interaction.

285 tin recruitment with lower dependence on the arrestin tail interaction.

286 oxin-interacting protein (TXNIP) is an alpha-arrestin that can bind to and inhibit the antioxidant pr

287 -aniline ring of fentanyl mediates muOR beta-arrestin through a novel M153 "microswitch" by synthesiz

288 Binding of arrestin to phosphorylated G-protein-coupled receptors (

289 al activation of G proteins and engages beta-arrestins to mediate distinct cellular signaling events.

290 is, supporting the previous notion that beta-arrestin translocation is of importance for cell migrati

291 17 (20), potently promotes D3R-mediated beta-arrestin translocation, G protein activation, and ERK1/2

292 in cones' responsiveness to light through an arrestin-translocation-independent mechanism.

293 ility of these peptides to bind and activate arrestins using a variety of biochemical and biophysical

294 llection of CCR5 phosphorylation mutants and arrestin variants to investigate how CCL5 analogs differ

295 om that adopted by the finger loop of visual arrestin when it couples to rhodopsin(8).

296 , one of which couples almost exclusively to arrestin, whereas the other also couples effectively to

297 otein-coupled receptors (GPCRs) recruit beta-arrestin, which desensitizes heterotrimeric G-protein si

298 family, signals through G proteins and beta-arrestins, which act as adaptors to regulate AT1R intern

299 st that the cooperative interactions of beta-arrestin with both the receptor and the phospholipid bil

300 echanisms underlying the interaction of beta-arrestin with GPCRs are much less understood.

301 ting the MOPr and marginally recruiting beta-arrestin, with no receptor internalization.