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1 inant-negative mutant version of arrestin-3 (beta-arrestin-2).
2 minal peptides competed for association with beta-arrestin 2.
3 d be rescued by cotransfection of cells with beta-arrestin 2.
4 s and receptor trafficking were regulated by beta-arrestin 2.
5 sent in dorsal root ganglion neurons lacking beta-arrestin 2.
6 through either G-protein alpha subunit 12 or beta-arrestin 2.
7 dopamine-mediated interaction of D2(L)R with beta-arrestin 2.
8 he association between active Smoothened and beta-arrestin 2.
9 signaling is not inhibited in the absence of beta-arrestin 2.
10 r induce different conformational changes in beta-arrestin 2.
11 str3 ciliary localization in neurons lacking beta-arrestin 2.
12 ffects on recruitment of the adapter protein beta-arrestin 2.
13 dent (PPM/PP2C) family and is independent of beta-arrestin 2.
14 tion to dendritic spines that is mediated by beta-arrestin-2.
15 2) "protective" effects) were independent of beta-arrestin-2.
16 eta-arrestin-1 and repress the expression of beta-arrestin-2.
17 animals were not observed in animals lacking beta-arrestin-2.
18 ver, DOI invokes the behavior independent of beta-arrestin-2.
19 sts from mice lacking beta-arrestin-1 and/or beta-arrestin-2.
20 2 cells, is fully functional in mice lacking beta-arrestin-2.
21 to biased signaling via either G proteins or beta-arrestin-2.
22 ient to confer MAPK sensitivity to the human beta-arrestin-2.
23 active state, leading to the recruitment of beta-arrestin-2.
24 of a molecular complex composed of TRAF6 and beta-arrestin-2.
26 been reported recently that T cells lacking beta-arrestin-2, a G protein-coupled receptor regulatory
28 otaxis, G protein-dependent and independent (beta-arrestin-2) activation, or secondary chemokine (CCL
29 t that strategies aimed at enhancing hepatic beta-arrestin 2 activity could prove useful for suppress
31 WT mice revealed that lithium disrupted the beta-arrestin-2/Akt/PP2A complex by directly inhibiting
32 r loss of one copy of the Gsk3b gene reduced beta-arrestin-2/Akt/PP2A complex formation in mice, whil
33 Thus, GSK-3 regulates the stability of the beta-arrestin-2/Akt/PP2A complex, and lithium disrupts t
34 beta-arrestin-2/AKT/protein phosphatase 2A (beta-arrestin-2/AKT/PP2A) complex that is known to be re
35 s, glycogen synthase kinase-3 (GSK-3), and a beta-arrestin-2/AKT/protein phosphatase 2A (beta-arresti
36 ssical function in receptor desensitization, beta-arrestin 2 also acts as a signaling intermediate th
37 esonance energy transfer)-based biosensor of beta-arrestin 2 and a combination of biased ligands and/
38 -60 min was blocked by depletion of cellular beta-arrestin 2 and beta-arrestin 1 by small interfering
43 signaling complex with the scaffold proteins beta-arrestin 2 and Ile Gln motif containing GTPase Acti
45 un-N-terminal kinase (JNK), which binds with beta-arrestin 2 and modulates the analgesic effects of m
46 Tsai identify two very different molecules--beta-arrestin 2 and Par-4, respectively--that unexpected
47 , a prototypical GPCR, dissociates eNOS from beta-arrestin 2 and promotes binding of beta-arrestin 2
48 uggest that a functional interaction between beta-arrestin 2 and Smoothened may be critical to regula
50 on inside Ift27(-/-) cilia and revealed that beta-arrestin 2 and the viral receptor CAR are candidate
52 te production by 48% (beta-arrestin-1), 71% (beta-arrestin-2), and 84% (beta-arrestins-1 and -2).
53 ed with beta-arrestin 1, 164 interacted with beta-arrestin 2, and 102 interacted with both beta-arres
56 nes derived from wild type, beta-arrestin 1, beta-arrestin 2, and beta-arrestin 1/2 knock-out mice.
57 p-regulation of GRK5 involves CB2 receptors, beta-arrestin 2, and ERK1/2 signaling because treatment
58 of morphine tolerance through regulation of beta-arrestin 2, and miR-365 upregulation provides a pro
59 imaging of green fluorescent protein-tagged beta-arrestin 2, and PathHunter beta-arrestin 2 assay.
62 tes with constitutive localization of PAR-2, beta-arrestin-2, and activated ERK1/2 to pseudopodia.
64 calcium, inhibited cAMP signaling, recruited beta-arrestin-2, and stimulated filamentous-actin accumu
65 sphorylation of the receptor, recruitment of beta-arrestin-2, and subsequent receptor internalization
67 1A (AT(1A)) receptor results in independent beta-arrestin 2- and G protein-mediated extracellular si
68 uncation analyses indicate that two sites in beta-arrestin 2 are involved in mediating its interactio
69 The nonvisual arrestins, beta-arrestin-1 and beta-arrestin-2, are multifunctional scaffolding protein
71 e characterize the conformational changes in beta-arrestin 2 (arrestin 3) by comparing the limited tr
72 amine-associated behaviors, thus implicating beta-arrestin 2 as a positive mediator of dopaminergic s
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
79 ted with rapid and transient inhibition of a beta-arrestin 2-associated pool of protein phosphatase 2
84 g either beta-arrestin 1 (beta arr1(-/-)) or beta-arrestin 2 (beta arr2(-/-)), agonist-induced DTS de
88 but not homologous) desensitization required beta-arrestin-2 (betaarr-2) because it was nearly abolis
89 marked inhibition of PAR1 signaling, whereas beta-arrestin 2 (betaarr2) was essentially inactive.
92 e have previously shown that adaptor protein beta-arrestin-2 (betaarr2) plays a crucial role in trans
93 posed to NT, beta-arrestin-1 (betaARR1), and beta-arrestin-2 (betaARR2) translocate to early endosome
94 coupled receptor kinase 5, thereby inducing beta-arrestin-2 biased PAR1 signaling by both APC and th
95 naling by thrombin, APC induces a protective beta-arrestin-2 biased PAR1 signaling by unknown mechani
96 main of protein C/APC is responsible for the beta-arrestin-2 biased PAR1 signaling independent of the
97 ructs revealed that EPCR occupancy initiates beta-arrestin-2 biased PAR1 signaling independent of the
100 -E54K) for 3 months with either TRV120067, a beta-arrestin 2-biased ligand of the angiotensin II rece
101 C3aR phosphorylation there was no change in beta-arrestin-2 binding or receptor desensitization.
102 s was associated with 74+/-2.4% decreases in beta-arrestin-2 binding, significantly reduced desensiti
105 kinase is abolished by depletion of cellular beta-arrestin 2 but is unaffected by the PKC inhibitor R
107 R antagonist and in MFS mice lacking AT1R or beta-arrestin 2, but not in MFS mice treated with an ang
110 he response blocked by depletion of cellular beta-arrestin 2 by small interfering RNA (beta-arrestin
111 in why the analog promotes higher amounts of beta-arrestin 2.CCR5 complexes, thereby increasing CCR5
112 We find a novel role for MAPK in the B2R/beta-arrestin-2 complex formation, receptor trafficking
113 lieve to be a new link between GSK-3 and the beta-arrestin-2 complex in mice and propose an integrate
114 it with high constitutive activity, the CCR1.beta-arrestin-2 complex is required for G protein-indepe
115 okine by the receptor suggests that the CCR1.beta-arrestin-2 complex may be related to a potential sc
116 of the behavioral phenotypes of mice lacking beta-arrestin 2 could be a result of altered JNK signali
126 the PAR(2)-enhanced inflammatory process is beta-arrestin-2 dependent, whereas the protective antico
127 These findings demonstrated p38 MAPK- and beta-arrestin 2-dependent cross-regulation between neuro
129 eptor-stimulated ERK1/2 activation was via a beta-arrestin 2-dependent pathway (suppressed by beta-ar
130 ences of ERK activation by the G protein and beta-arrestin 2-dependent pathways were also distinct.
131 ia both G protein-dependent and independent (beta-arrestin 2-dependent) signaling, but the role of th
140 dependent ERK1/2 activation, indicating that beta-arrestin 2 expression confers ERK1/2 activation via
141 ely, suppression of beta-arrestin 1, but not beta-arrestin 2, expression by using RNA interference le
143 al changes associated with the transition of beta-arrestin 2 from its basal inactive conformation to
145 (GRK2) leads to phosphorylation of Smo, and beta-arrestin 2 fused to green fluorescent protein inter
146 We identified elevated expression of the beta-arrestin 2 gene (Arrb2) in the striatum and the hip
147 d in vivo murine models, we demonstrate that beta-arrestin-2 gene ablation augments beta-agonist-medi
148 tized mice having a targeted deletion of the beta-arrestin-2 gene do not accumulate T lymphocytes in
149 differentially regulate beta-arrestin-1 and beta-arrestin-2 gene expression in multiple cell types.
152 in signaling but does lead to recruitment of beta-arrestin 2-GFP and activation of extracellular sign
153 antly, hepatocyte-specific overexpression of beta-arrestin 2 greatly reduced hepatic GCGR signaling a
154 py, the two mutant receptors interacted with beta-arrestin 2-green fluorescent protein with much lowe
158 Release of the C terminus from the rest of beta-arrestin 2 has functional consequences in that it i
159 n also leads to release of the C terminus of beta-arrestin 2; however, heparin and V(2)R-pp have diff
160 n contrast, knockdown or genetic ablation of beta-arrestin 2 in an insulin-secreting cell line and mo
161 In contrast, we show the critical role of beta-arrestin 2 in CB1 receptor internalization upon tre
162 inactivation of the GPCR-associated protein beta-arrestin 2 in hepatocytes of adult mice results in
163 n of exon 7-associated C-terminal tails with beta-arrestin 2 in morphine-induced desensitization and
165 mass spectrometry (MALDI-TOF MS) profiles of beta-arrestin 2 in the presence of a phosphopeptide (V(2
167 re, we show that the functional knockdown of beta-arrestin 2 in zebrafish embryos recapitulates the m
169 These findings establish a key role for beta-arrestin-2 in mediating cellular cytoprotective fun
170 Our studies demonstrate unique functions of beta-arrestin-2 in NMDAR-mediated dendritic spine and sy
173 8alpha, and AKT1, whereas down-regulation of beta-arrestin-2 increased phosphorylation of AKT1 in bot
174 n by the epidermal growth factor receptor (a beta-arrestin 2 independent pathway) had no effect on iN
175 o determine the effect of beta-arrestin-1 or beta-arrestin-2 inhibition or gene ablation on signaling
177 discover that excessive Krz, the Drosophila beta-arrestin 2, inhibits Smo sumoylation and prevents S
179 (PKA)-activated PDE4D3, scaffolded through a beta-arrestin 2 interaction with Ser(704) of the recepto
183 e of the cascades that could be regulated by beta-arrestin 2 is cJun-N-terminal kinase (JNK), which b
186 ed by GRKs in cells and that in consequence, beta-arrestin 2 is localized to the plasma membrane.
187 synthase (eNOS), and that S-nitrosylation of beta-arrestin 2 is promoted by endogenous S-nitrosogluth
188 This report provides the first evidence that beta-arrestin-2 is required for the manifestation of all
189 ory motif is conserved between rat and mouse beta-arrestin-2, it is surprisingly not conserved in hum
190 PV1 desensitization in primary cultures from beta-arrestin-2 knock-out mice compared with wild type.
194 lgesic response with reduced side effects in beta-arrestin-2 knockout mice compared to wild-type mice
197 Overexpression of either beta-arrestin 1 or beta-arrestin 2 led to marked inhibition of NF-kappaB ac
198 nduced NF-kappaB activation, suggesting that beta-arrestin 2 may recruit CARMA3 to LPA receptors.
201 to Gq/11, GPR40 is functionally linked to a beta-arrestin 2-mediated insulinotropic signaling axis.
202 the existence of independent G protein- and beta-arrestin 2-mediated pathways leading to ERK1/2 acti
210 e cellular complement of beta-arrestin-1 and beta-arrestin-2 occur in many human diseases, and their
212 n of beta-arrestin-1 with its counterpart on beta-arrestin-2 or using a specific TAT-P1 peptide to bl
213 we found that mice lacking beta-arrestin 1, beta-arrestin 2, or AT1R were unable to generate a Frank
216 hifted the bias of several mu opioids toward beta-arrestin 2 over G protein activation compared with
220 ulatory motif in the hinge domain of the rat beta-arrestin-2 (PET(178)P), but not rat beta-arrestin-1
221 ed with in vitro kinase assays revealed that beta-arrestin-2 phosphorylation on Ser14 and Thr276 is e
222 demonstrates that C5aR2 ligation initiates a beta-arrestin-2-, PI3K-, and ERK-dependent signaling pat
223 Our data demonstrate that although Src and beta-arrestin 2 play essential roles in beta2-adrenergic
227 , we have recently shown that GRK2, GRK3 and beta-arrestin-2 promote C3a receptor (C3aR) desensitizat
228 n with unlabeled TSH; however, expression of beta-arrestin-2 promoted TSHR internalization that was i
231 and ziprasidone all potently antagonize the beta-arrestin 2 recruitment to D2(L)R induced by quinpir
232 nd leads to receptor internalization and the beta-arrestin 2 recruitment with potency comparable to t
233 Both in G protein-mediated pathways and in beta-arrestin 2 recruitment, no ligand-independent activ
235 0.34 +/- 0.01 hours for adrenaline-mediated beta-arrestin-2 recruitment and GFP-beta2 internalizatio
236 Ser470 participate in C3aR desensitization, beta-arrestin-2 recruitment and inhibition of NF-kappaB
237 mine the role of receptor phosphorylation on beta-arrestin-2 recruitment and RBL-2H3 cells for functi
239 show a strong, predominantly NTS1R-mediated beta-arrestin-2 recruitment at the D2R/NTS1R-coexpressin
240 he slower rate for C26 resulted in levels of beta-arrestin-2 recruitment increasing up to 4-hour agon
241 inct conformations of a 7TMR associated with beta-arrestin-2 recruitment or G-protein coupling and va
242 sequently represent biased agonists favoring beta-arrestin-2 recruitment over canonical G protein act
243 f Ca(2)(+) mobilization, beta-arrestin-1 and beta-arrestin-2 recruitment, and extracellular signal-re
244 nous ligand adrenaline in cAMP accumulation, beta-arrestin-2 recruitment, and receptor internalizatio
245 ined with other functional readouts, such as beta-arrestin-2 recruitment, cAMP accumulation, and calc
246 azines (1,4-DAPs) behaved as antagonists for beta-arrestin-2 recruitment, implying significant ligand
251 d dynamic S-nitrosylation/denitrosylation of beta-arrestin 2 regulates stimulus-induced GPCR traffick
253 and murine model systems, knockdown or KO of beta-arrestin-2 relative to control missense small inter
254 ytosis, mediated by a novel interaction with beta arrestin-2, results in decreased TGF-beta signaling
257 ur results provide the genetic evidence that beta-arrestin 2 serves as a positive regulator in NF-kap
259 ontaining protein tyrosine phosphatase 2 and beta-arrestin 2, showed higher inhibition of lipid raft
260 eatment with CB2 shRNA lentiviral particles, beta-arrestin 2 shRNA lentiviral particles, or ERK1/2 in
262 hat binds to APJ, activates the Galphai1 and beta-arrestin-2 signaling pathways, and induces receptor
265 n by the mutant receptors was insensitive to beta-arrestin 2 small interfering RNA but was reduced mo
266 -arrestin 2-dependent pathway (suppressed by beta-arrestin 2 small interfering RNA), whereas the rest
267 h H89, an inhibitor of protein kinase A, and beta-arrestin 2 small interfering RNA, respectively.
271 not most other mu agonists, in mice lacking beta-arrestin 2, suggest that this scaffolding protein r
272 ted mutagenesis and cells or tissues lacking beta-arrestin 2 suggests a role for these desensitizatio
273 imetic residue in both the rat and the human beta-arrestin-2 (T/K178D) significantly stabilizes B2R/b
275 CRF receptor (CRF1) with the Gs protein and beta-arrestin 2 that would render females more responsiv
276 , we observed that in MEF cells deficient in beta-arrestin 2 the internalization of the beta2-adrener
279 from beta-arrestin 2 and promotes binding of beta-arrestin 2 to clathrin heavy chain/beta-adaptin, th
280 ed enhanced green fluorescent protein (EGFP)-beta-arrestin 2 to the plasma membrane, whereas the SA3
281 ivation of M3-Rs inhibits the recruitment of beta-arrestin-2 to ORs, resulting in a potentiation of o
282 , benzamide 7b, that promotes recruitment of beta-arrestin-2 to the microOR and receptor internalizat
283 that 1c does not promote the recruitment of beta-arrestin-2 to the microOR or receptor internalizati
284 kinorin, does not promote the recruitment of beta-arrestin-2 to the muOR and does not lead to recepto
289 trast, ERK1/2 activation in cells expressing beta-arrestin 2 was predominantly EGF receptor-independe
291 ernalization of receptors and recruitment of beta-arrestin 2 were unaffected by the loss of 187 glyco
293 the mu opioid receptor but failed to recruit beta-arrestin-2, which is associated with opioid side ef
294 was significantly inhibited by knockdown of beta-arrestin 2 with siRNA in cytokine-treated HLMVECs o
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
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