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1 n the Arg(363)-Arg(393) region in the bovine beta-arrestin 1.
2 eceptor selectivity for beta-arrestin 2 over beta-arrestin 1.
3 rectal cancer cells expressing WT and mutant beta-arrestin 1.
4 ansfection with the scaffold/adapter protein beta-arrestin 1.
5 appaB, IkappaBalpha, as a binding partner of beta-arrestin 1.
6 Gbetagamma and c-Src, and possibly involves beta-arrestin 1.
7 ctivation was enhanced by over-expression of beta-arrestin 1.
8 a-arrestin 2 to be 100-fold more potent than beta-arrestin 1.
9 cadaverine, a mutant dynamin I, and a mutant beta-arrestin 1.
10 llowing the overexpression of either GRK2 or beta-arrestin 1.
11 or kinases (GRKs) 2, 3, 5, and 6, as well as beta-arrestin 1.
12 were equally effective at coupling to Gi and beta-arrestin-1.
13 e rescued by ectopic expression of wild-type beta-arrestin-1.
14 esponding to the antibody-binding epitope on beta-arrestin-1.
15 rt, caused by activatory signals mediated by beta-arrestin-1.
16 licated in maintaining the inactive state of beta-arrestin-1.
17 hosphorylated vasopressin-2 receptor tail to beta-arrestin-1.
18 o functionally and conformationally activate beta-arrestin-1.
19 gnizes the phosphopeptide-activated state of beta-arrestin-1.
20 as being critical to nuclear localization of beta-arrestin-1.
21 by LC tandem MS, 71 proteins interacted with beta-arrestin 1, 164 interacted with beta-arrestin 2, an
22 oprecipitation of the PAFR and clathrin with beta-arrestin-1, 2) fluorescent resonance energy transfe
25 could indeed be detected in IL-8-stimulated beta-arrestin 1/2 knockout cells, and cytoplasmic Rac wa
26 FLAG epitope-tagged beta-arrestin 2 into the beta-arrestin 1/2 null background restored EGF receptor-
29 acid did not stimulate TGR5 association with beta-arrestin 1/2 or G protein-coupled receptor kinase (
30 al-regulated kinase 1 and 2 phosphorylation, beta-arrestin 1/2 recruitment, and MOP trafficking, and
32 minant-negative form of the beta-arrestin 1, beta-arrestin 1 (319-418), blocked agonist-mediated inte
33 ulated inositol phosphate production by 48% (beta-arrestin-1), 71% (beta-arrestin-2), and 84% (beta-a
34 both G-protein-coupled receptor-kinase 2 and beta-arrestin-1, a G-protein-coupled receptor adaptor pr
36 carcinoma cells, the increased expression of beta-arrestin-1 after glucocorticoid treatment impairs G
37 ated that Galpha(i), betagamma subunits, and beta-arrestin-1 all play a critical role in IGF-I mitoge
39 oexpressed isoforms of beta-arrestin (termed beta arrestin 1 and 2) are highly similar in amino acid
40 -2 and show, in vitro, that these domains in beta-arrestin 1 and 2 interact equally well with AP-2 in
43 incubated with progastrin or Bmp2; levels of beta-arrestin 1 and 2 were knocked down using small inte
44 To better define differences in the roles of beta-arrestin 1 and 2, we prepared mouse embryonic fibro
45 mice and cultured human cells via CCK2R- and beta-arrestin 1 and 2-dependent suppression of Bmp2 sign
48 activate RhoA, the concurrent recruitment of beta-arrestin 1 and activation of G(alphaq/11) leads to
50 alling complex was made by docking activated beta-arrestin 1 and beta2AR crystal structures into the
52 /11) in response to ET-1 stimulation, and 2) beta-arrestin 1 and Src kinase form a molecular complex
53 onse involved formation of a complex between beta-arrestin 1 and the Akt phosphatase PHLPP2, and acti
55 and 3) rapid and transient redistribution of beta-arrestin-1 and -2 from the cytosol to the plasma me
56 immunoreactive Galphaq/11, GRK-2 and -3, and beta-arrestin-1 and -2 in a subpopulation of neurons.
57 tion of NK1-R, Galphaq/11, GRK-2 and -3, and beta-arrestin-1 and -2 in cultured myenteric neurons.
58 ne, followed by a striking redistribution of beta-arrestin-1 and -2 to endosomes containing the NK1-R
61 erize the cellular localization of wild type beta-arrestin-1 and a series of N domain mutants to dete
62 that glucocorticoids differentially regulate beta-arrestin-1 and beta-arrestin-2 gene expression in m
63 Alterations in the cellular complement of beta-arrestin-1 and beta-arrestin-2 occur in many human
64 luding stimulation of Ca(2)(+) mobilization, beta-arrestin-1 and beta-arrestin-2 recruitment, and ext
67 Furthermore, there was significantly more beta-arrestin-1 and E2F1 associated with these promoters
68 with nicotine led to enhanced recruitment of beta-arrestin-1 and E2F1 on vimentin, fibronectin, and Z
69 mulation to ERK activation and lipolysis; 3) beta-arrestin-1 and G alpha(q/11) can mediate TNFalpha-i
70 uitin content of IRS-1, suggesting that both beta-arrestin-1 and IRS-1 competitively bind to Mdm2.
71 -P1 peptide to block the interaction between beta-arrestin-1 and PLCgamma abolishes TRV120027-induced
72 -arrestin-1 content due to ubiquitination of beta-arrestin-1 and proteosome-mediated degradation.
73 gation requires CME and causes engagement of beta-arrestin-1 and recruitment of a p38 MAPK signalosom
74 oid receptor (GR) to induce the synthesis of beta-arrestin-1 and repress the expression of beta-arres
75 can be enhanced by the presence of GRK2 and beta-arrestin-1 and show that these molecules have multi
80 ciprocal effects of down-regulated levels of beta-arrestins 1 and 2 are primarily due to differences
86 rminal peptide competed for association with beta-arrestin 1, and phosphorylated central or distal C-
87 uitination of TRPV4, a process that requires beta-arrestin 1, and subsequently to internalization and
88 ansfer-positive interactions among the PAFR, beta-arrestin-1, and clathrin, 3) recruitment and activa
89 eptor (IGF-IR) endocytosis is facilitated by beta-arrestin-1, and internalization is necessary for IG
90 yclase signaling, to a strong recruitment of beta-arrestin-1, and to a positive cross talk of D1R and
93 2 on beta-arrestin and the amino terminus of beta-arrestin-1 are required for this effect of beta-arr
96 re, our data implicate a functional role for beta-arrestin 1 as a mediator of cellular migration and
97 R signaling, and highlight the importance of beta-arrestin-1 as a target molecule for this desensitiz
98 munoprecipitation experiments, we found that beta-arrestin 1 associated with the ETA receptor in an a
99 hosphorylation coincided with an increase in beta-arrestin 1-associated PGES3 and an arrestin-depende
100 p85 within the pseudopodia, suggesting that beta-arrestin-1 association with PI3K may spatially rest
102 eumococci-induced colocalization of PAFr and beta-arrestin 1 at the plasma membrane of endothelial ce
103 Arenas et al (2014) describe a novel role of beta-arrestin-1 at the IS periphery: endocytosis of TCRs
106 ryonic fibroblast (MEF) cells lacking either beta-arrestin 1 (beta arr1(-/-)) or beta-arrestin 2 (bet
107 ac macromolecular complex involving VDCC and beta-arrestin 1 (beta-Arr1) into clathrin-coated vesicle
108 a novel bypass mechanism through which ETAR/beta-arrestin-1 (beta-arr1, ARRB1) links Wnt signaling t
109 However, a dominant-negative form of the beta-arrestin 1, beta-arrestin 1 (319-418), blocked agon
111 -dependent myofilament Ca(2+) sensitivity in beta-arrestin 1, beta-arrestin 2, and AT1R knockout mice
112 ing fibroblast lines derived from wild type, beta-arrestin 1, beta-arrestin 2, and beta-arrestin 1/2
113 ive hemodynamics, we found that mice lacking beta-arrestin 1, beta-arrestin 2, or AT1R were unable to
115 ular loop (V2R(DeltaICL3)) can interact with beta-arrestin 1 (betaarr1) only through the phosphorylat
119 dependent aldosterone production mediated by beta-arrestin-1 (betaarr1), a universal heptahelical rec
120 we show that in NCM460 cells exposed to NT, beta-arrestin-1 (betaARR1), and beta-arrestin-2 (betaARR
122 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
124 t receptor exhibits reduced association with beta-arrestin 1 but continues to exhibit association wit
125 A mutants of CXCR2 exhibit normal binding to beta-arrestin 1 but exhibit decreased binding to adaptin
127 ablate tight junctions consistent with EMT; beta-arrestin-1, but not beta-arrestin-2, was required f
131 These results show that the prostaglandin E/beta-arrestin 1/c-Src signaling complex is a crucial ste
132 association of a prostaglandin E receptor 4/beta-arrestin 1/c-Src signaling complex resulting in the
133 a clearly show that both visual arrestin and beta-arrestin 1 can bind to monomeric rhodopsin and stab
134 In summary, we have found the following: (i) beta-arrestin-1 can alter insulin signaling by inhibitin
135 molecules in the TNFalpha action cascade; 2) beta-arrestin-1 can couple TNFalpha stimulation to ERK a
136 beta-arrestin-dependent mechanism, and that beta-arrestin-1 can directly associate with and inhibit
137 ponent G alpha(q/11) and the adapter protein beta-arrestin-1 can function as signaling molecules in t
138 vity blocks PAR-2-stimulated chemotaxis, and beta-arrestin-1 colocalizes with p85 within the pseudopo
139 x shows marked conformational differences in beta-arrestin-1 compared to its inactive conformation.
140 ing and purifying a functional human beta2AR-beta-arrestin-1 complex that allowed us to visualize its
141 phospho-barcodes are translated to specific beta-arrestin-1 conformations and direct selective signa
143 es an approximately 50% decrease in cellular beta-arrestin-1 content due to ubiquitination of beta-ar
145 duced proteasomal degradation of IRS-1; (ii) beta-arrestin-1 decreases the rate of ubiquitination of
146 n and enhanced IL-10 and IL-22 production in beta-arrestin-1-deficient mice likely lead to attenuated
148 inositol phosphate signaling while enhancing beta-arrestin-1-dependent stimulation of the MAPK pathwa
151 dentify the interaction kinetics of CB1R and beta-arrestin 1 during their endocytic trafficking as di
153 lays important roles in the nucleus, but how beta-arrestin-1 enters the nucleus remains unclear becau
154 podocytes and hyperplastic lesion formation; beta-arrestin-1 expression increased in visceral podocyt
156 lasma membrane that also contained Rab5a and beta-arrestin 1, followed by rapid recycling of the NK1R
157 strate that ERK1/2 activation is mediated by beta-arrestin 1 from receptors localized exclusively at
158 rticoid response elements in intron-1 of the beta-arrestin-1 gene and intron-11 of the beta-arrestin-
159 in insulin-treated cells in which endogenous beta-arrestin-1 had been downregulated rescued IGF-I- an
160 physical association between the GLP-1 R and beta-arrestin-1 in cultured INS-1 pancreatic beta cells.
164 oimmunoprecipitated with follicular membrane beta-arrestin-1 in response to LH/CG R activation compar
165 ether, these studies reveal a novel role for beta-arrestin-1 in the growth and metastasis of NSCLC.
169 btypes differentially regulate ASM GPCRs and beta-arrestin-1 inhibition represents a novel approach t
170 Small interfering RNA-mediated knockdown of beta-arrestin-1 inhibits TNFalpha-induced tyrosine phosp
177 In the present study, we determined whether beta-arrestin-1 is involved in insulin-induced insulin r
178 we demonstrate that the scaffolding protein beta-arrestin-1 is necessary for nicotine-mediated induc
179 work, we found that beta-arrestin 2, but not beta-arrestin 1, is required for LPA-induced NF-kappaB a
180 imulates lipolysis in 3T3-L1 adipocytes, and beta-arrestin-1 knockdown blocks the effects of TNFalpha
183 rotein-1 and matrix metalloproteinase 3, and beta-arrestin-1 knockdown inhibited both of these effect
185 To this end, we subjected wild-type (WT) and beta-arrestin-1 knockout (beta-arr-1(-/-)) mice to colit
186 on IRS-1 degradation; and (iv) inhibition of beta-arrestin-1 leads to enhanced IRS-1 degradation and
187 ic insulin treatment down-regulates cellular beta-arrestin 1 levels, leading to a marked impairment i
188 h these promoters in human NSCLC tumors, and beta-arrestin-1 levels correlated with vimentin and fibr
192 Arg323 and Lys409 residues were required for beta-arrestin-1-mediated sustained ERK phosphorylation a
193 th phosphoinositide (PI) hydrolysis and with beta-arrestin-1-mediated sustained extracellular signal-
194 -induced signaling mechanism for CB1 wherein beta-arrestin 1 mediates short term signaling to ERK1/2
196 -1 action, showing that the scaffold protein beta-arrestin-1 mediates the effects of GLP-1 to stimula
198 e of Cell, Kang et al. provide evidence that beta-arrestin 1 moves to the nucleus in response to GPCR
199 Expression of a phosphorylation-independent beta-arrestin 1 mutant (R169E) significantly rescued the
203 hese results demonstrate a critical role for beta-arrestin-1 nuclear localization in scaffolding and
207 Second, overexpression of arrestin 2 or 3 (beta-arrestin 1 or 2) abolished the V2 receptor-mediated
211 gnals via beta-arrestin, and in mice lacking beta-arrestin-1 or -2, KP-triggered GnRH secretion is si
217 However, upon coexpression of arrestin-2 (beta-arrestin-1) or arrestin-3 (beta-arrestin-2), intern
219 in membrane-associated beta-arrestin-1, that beta-arrestin-1 participates in agonist-dependent desens
222 Taken together, these studies indicate that beta-arrestin-1 plays a role in GLP-1 signaling leading
223 A mounting body of evidence suggests that beta-arrestin-1 plays important roles in the nucleus, bu
226 G protein-coupled receptor kinase 3 (GRK3), beta-arrestin-1, Pyk2, and focal adhesion kinase (FAK).
227 With its phosphate-binding concave surface, beta-arrestin-1 'reads' the message in the receptor phos
228 ptor in an agonist-dependent manner and that beta-arrestin 1 recruited Src kinase to a molecular comp
229 hermore, D1R or D3R antagonists counteracted beta-arrestin-1 recruitment and MAPK activation induced
230 We conclude that PAF signaling requires CME, beta-arrestin-1 recruitment of a p38 MAPK signalosome, a
231 xpression of a dominant negative fragment of beta-arrestin-1 reduces PAR-2-stimulated internalization
239 restin-1 was knocked down by transfection of beta-arrestin-1 small interfering RNA, insulin-induced I
241 rough mGlu1a receptors require expression of beta-arrestin-1, suggesting a possible role for receptor
243 atterns induce distinct structural states of beta-arrestin-1 that are coupled to distinct arrestin fu
244 varian follicles contain membrane-associated beta-arrestin-1, that beta-arrestin-1 participates in ag
245 follicular membranes unexpectedly contained beta-arrestin-1, the role of arrestins in desensitizatio
246 ategy to retrieve AT(1)R-engaged isoforms of beta-arrestin 1 to confirm direct interaction of fragmen
247 10 nM) induced translocation of the NK1R and beta-arrestin 1 to perinuclear sorting endosomes contain
248 al reconstructions reveal bimodal binding of beta-arrestin 1 to the beta2AR, involving two separate s
251 protein-coupled receptor kinase-2 (GRK2) and beta-arrestin-1 to regulate the phosphorylation state an
252 Within this paradigm, M3D-arr recruited beta-arrestin-1 to the plasma membrane, and promoted pho
253 tion of CB1-GFP with red fluorescent protein-beta-arrestin 1 upon ORG27569 treatment using confocal m
254 cterize the interactions between beta2AR and beta-arrestin 1 using hydrogen-deuterium exchange mass s
260 ynergistically enhanced by cotransfection of beta-arrestin-1, which had no effect on m2 mAChR functio
261 iation was inhibited to overexpression of WT beta-arrestin-1, which led by decreased ubiquitin conten
262 ues suggest engagement of the finger loop of beta-arrestin 1 with the seven-transmembrane core of the
264 ound a marked decrease in the association of beta-arrestin-1 with the IGF-IR and a 55% inhibition of
265 en CFP-iNOS and beta-arrestin 2-YFP (but not beta-arrestin 1-YFP) that increased 3-fold after B1R sti
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