Relevant bibliographies by topics / ?-arrestin

Academic literature on the topic '?-arrestin'

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Published: 4 June 2021
Last updated: 10 March 2023

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Journal articles on the topic "?-arrestin"

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Santini, F., R. B. Penn, A. W. Gagnon, J. L. Benovic, and J. H. Keen. "Selective recruitment of arrestin-3 to clathrin coated pits upon stimulation of G protein-coupled receptors." Journal of Cell Science 113, no. 13 (July 1, 2000): 2463–70. http://dx.doi.org/10.1242/jcs.113.13.2463.

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Non-visual arrestins (arrestin-2 and arrestin-3) play critical roles in the desensitization and internalization of many G protein-coupled receptors. In vitro experiments have shown that both non-visual arrestins bind with high and approximately comparable affinities to activated, phosphorylated forms of receptors. They also exhibit high affinity binding, again of comparable magnitude, to clathrin. Further, agonist-promoted internalization of many receptors has been found to be stimulated by exogenous over-expression of either arrestin2 or arrestin3. The existence of multiple arrestins raises the question whether stimulated receptors are selective for a specific endogenous arrestin under more physiological conditions. Here we address this question in RBL-2H3 cells, a cell line that expresses comparable levels of endogenous arrestin-2 and arrestin-3. When (beta)(2)-adrenergic receptors are stably expressed in these cells the receptors internalize efficiently following agonist stimulation. However, by immunofluorescence microscopy we determine that only arrestin-3, but not arrestin-2, is rapidly recruited to clathrin coated pits upon receptor stimulation. Similarly, in RBL-2H3 cells that stably express physiological levels of m1AChR, the addition of carbachol selectively induces the localization of arrestin-3, but not arrestin-2, to coated pits. Thus, this work demonstrates coupling of G protein-coupled receptors to a specific non-visual arrestin in an in vivo setting.
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2

JAHNS, Roland, Franck BORGESE, Sabine LINDENTHAL, Annette STRAUB, René MOTAIS, and Bruno FIÉVET. "Trout red blood cell arrestin (TRCarr), a novel member of the arrestin family: cloning, immunoprecipitation and expression of recombinant TRCarr." Biochemical Journal 316, no. 2 (June 1, 1996): 497–506. http://dx.doi.org/10.1042/bj3160497.

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Arrestins are cytosolic proteins involved in the desensitization of G-protein-coupled receptors. We report the cloning of trout red blood cell arrestin which shows 76, 82 and 52% identity with bovine β-arrestin1, β-arrestin2 and retinal arrestin respectively. Antibodies were generated against the C-terminus of trout red blood cell arrestin. These antibodies detected arrestin in erythrocyte cytosol and were able to precipitate the native protein. The Na+/H+ antiporter of trout red blood cell is activated by β-adrenergic stimulation and is then desensitized whereas the transmembrane signalling pathway is not. To investigate the subcellular distribution of arrestin on β-adrenergic activation and desensitization of the antiporter, precipitation experiments were carried out on trout erythrocytes. A desensitization-dependent shift in cytosolic arrestin to the membranes could not be detected using the immunoprecipitation technique but we cannot exclude the possibility that a small number of cytosolic arrestins might be involved in the regulation of membrane proteins in trout erythrocyte. Recombinant trout arrestin was produced in a protease-deficient Escherichia coli strain and its functionality was tested in a reconstituted rhodopsin assay. The recombinant protein provides a suitable tool for investigating the target for arrestin in trout red blood cell, which still remains to be identified.
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Rakib, Ahmed, Taslima Akter Eva, Saad Ahmed Sami, Saikat Mitra, Iqbal Hossain Nafiz, Ayan Das, Abu Montakim Tareq, et al. "Beta-Arrestins in the Treatment of Heart Failure Related to Hypertension: A Comprehensive Review." Pharmaceutics 13, no. 6 (June 5, 2021): 838. http://dx.doi.org/10.3390/pharmaceutics13060838.

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Heart failure (HF) is a complicated clinical syndrome that is considered an increasingly frequent reason for hospitalization, characterized by a complex therapeutic regimen, reduced quality of life, and high morbidity. Long-standing hypertension ultimately paves the way for HF. Recently, there have been improvements in the treatment of hypertension and overall management not limited to only conventional medications, but several novel pathways and their pharmacological alteration are also conducive to the treatment of hypertension. Beta-arrestin (β-arrestin), a protein responsible for beta-adrenergic receptors’ (β-AR) functioning and trafficking, has recently been discovered as a potential regulator in hypertension. β-arrestin isoforms, namely β-arrestin1 and β-arrestin2, mainly regulate cardiac function. However, there have been some controversies regarding the function of the two β-arrestins in hypertension regarding HF. In the present review, we try to figure out the paradox between the roles of two isoforms of β-arrestin in the treatment of HF.
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4

Li, Dongjun, and Donna Woulfe. "Arrestin-2 Differentially Regulates PAR4 and P2Y12 Receptor Signaling in Platelets." Blood 112, no. 11 (November 16, 2008): 110. http://dx.doi.org/10.1182/blood.v112.11.110.110.

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Abstract Arrestins play important roles in the function of G Protein-Coupled Receptors (GPCRs) in many cells, but their roles in platelets remain uncharacterized. While the classical role of arrestins is considered to be the internalization and desensitization of GPCRs, more recent studies suggest that arrestins can serve as molecular scaffolds to recruit phosphatidyl inositol-3 kinases (PI3Ks) to GPCRs and promote PI3K-dependent signaling. Due to the multifunctional role of arrestins, we sought to determine whether arrestins regulate Akt activation in platelets and thrombosis in living animals. Co-immunoprecipitation experiments indicate that arrestin-2 associates with PAR4 in thrombin-treated platelets and P2Y12 in ADP-treated platelets, but neither receptor in resting cells. Interestingly, association of arrestin-2 with PAR4 was also stimulated by ADP and PAR4-induced association of arrestin with PAR4 was inhibited by P2Y12 antagonists or apyrase. To determine the functional role of arrestin-2 in platelets, ADP- and thrombin receptor-stimulated Akt phosphorylation was compared in platelets from arrestin-2 knock-out versus WT mice. Akt phosphorylation stimulated by 0.8 mM AYPGKF PAR4 agonist peptide was reduced by an average of 77% in arrestin-2 knock-out platelets compared to WT controls (significantly different, p=0.007, n=3 in each group), but ADP-stimulated Akt phosphorylation was unaffected (p=.38, n=3 each). PAR4-stimulated fibrinogen binding was also reduced in arrestin2−/− platelets (by 58.5% in 1 mM AYPGKF-stimulated platelets compared to WT controls), whereas ADP-stimulated fibrinogen binding was not. Finally, arrestin2 knock-out mice were less sensitive to ferric chloride-induced thrombosis than WT mice: 55% of WT mice (n-=9) formed occlusive thrombi after 2min15sec exposure of the carotid artery to 10% ferric chloride, whereas only 11% of WT mice (n=9) formed occlusive thrombi under the same conditions. In conclusion, arrestin-2 associates with both PAR4 and P2Y12 receptors, but differentially regulates their signaling to Akt and fibrinogen binding and appears to play a net positive role in regulating thrombosis in vivo.
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Morris, Gavin E., Carl P. Nelson, Paul J. Brighton, Nicholas B. Standen, R. A. John Challiss, and Jonathon M. Willets. "Arrestins 2 and 3 differentially regulate ETA and P2Y2 receptor-mediated cell signaling and migration in arterial smooth muscle." American Journal of Physiology-Cell Physiology 302, no. 5 (March 1, 2012): C723—C734. http://dx.doi.org/10.1152/ajpcell.00202.2011.

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Overstimulation of endothelin type A (ETA) and nucleotide (P2Y) Gαq-coupled receptors in vascular smooth muscle causes vasoconstriction, hypertension, and, eventually, hypertrophy and vascular occlusion. G protein-coupled receptor kinases (GRKs) and arrestin proteins are sequentially recruited by agonist-occupied Gαq-coupled receptors to terminate phospholipase C signaling, preventing prolonged/inappropriate contractile signaling. However, these proteins also play roles in the regulation of several mitogen-activated protein kinase (MAPK) signaling cascades known to be essential for vascular remodeling. Here we investigated whether different arrestin isoforms regulate endothelin and nucleotide receptor MAPK signaling in rat aortic smooth muscle cells (ASMCs). When intracellular Ca2+ levels were assessed in isolated ASMCs loaded with Ca2+-sensitive dyes, P2Y2 and ETA receptor desensitization was attenuated by selective small-interfering (si)RNA-mediated depletion of G protein-coupled receptor kinase 2 (GRK2). Using similar siRNA techniques, knockdown of arrestin2 prevented P2Y2 receptor desensitization and enhanced and prolonged p38 and ERK MAPK signals, while arrestin3 depletion was ineffective. Conversely, arrestin3 knockdown prevented ETA receptor desensitization and attenuated ET1-stimulated p38 and ERK signals, while arrestin2 depletion had no effect. Using Transwell assays to assess agonist-stimulated ASMC migration, we found that UTP-stimulated migration was markedly attenuated following arrestin2 depletion, while ET1-stimulated migration was attenuated following knockdown of either arrestin. These data highlight a differential arrestin-dependent regulation of ETA and P2Y2 receptor-stimulated MAPK signaling. GRK2 and arrestin expression are essential for agonist-stimulated ASMC migration, which, as a key process in vascular remodeling, highlights the potential roles of GRK2 and arrestin proteins in the progression of vascular disease.
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Cao, Yubo, Sahil Kumar, Yoon Namkung, Laurence Gagnon, Aaron Cho, and Stéphane A. Laporte. "Angiotensin II type 1 receptor variants alter endosomal receptor–β-arrestin complex stability and MAPK activation." Journal of Biological Chemistry 295, no. 38 (July 23, 2020): 13169–80. http://dx.doi.org/10.1074/jbc.ra120.014330.

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The angiotensin II (AngII) type 1 receptor (AT1R), a member of the G protein–coupled receptor (GPCR) family, signals through G proteins and β-arrestins, which act as adaptors to regulate AT1R internalization and mitogen-activated protein kinase (MAPK) ERK1/2 activation. β-arrestin–dependent ERK1/2 regulation is the subject of important studies because its spatiotemporal control remains poorly understood for many GPCRs, including AT1R. To study the link between β-arrestin–dependent trafficking and ERK1/2 signaling, we investigated three naturally occurring AT1R variants that show distinct receptor–β-arrestin interactions: A163T, T282M, and C289W. Using bioluminescence resonance energy transfer (BRET)–based and conformational fluorescein arsenical hairpin–BRET sensors coupled with high-resolution fluorescence microscopy, we show that all AT1R variants form complexes with β-arrestin2 at the plasma membrane and efficiently internalize into endosomes upon AngII stimulation. However, mutant receptors imposed distinct conformations in β-arrestin2 and differentially impacted endosomal trafficking and MAPK signaling. Notably, T282M accumulated in endosomes, but its ability to form stable complexes following internalization was reduced, markedly impairing its ability to co-traffic with β-arrestin2. We also found that despite β-arrestin2 overexpression, T282M's and C289W's residency with β-arrestin2 in endosomes was greatly reduced, leading to decreased β-arrestin–dependent ERK1/2 activation, faster recycling of receptors to the plasma membrane, and impaired AngII-mediated proliferation. Our findings reveal that naturally occurring AT1R variants alter the patterns of receptor/β-arrestin2 trafficking and suggest conformationally dependent β-arrestin–mediated MAPK activation as well as endosomal receptor–β-arrestin complex stabilization in the mitogenic response of AT1R.
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Zarca, Aurélien, Claudia Perez, Jelle van den Bor, Jan Paul Bebelman, Joyce Heuninck, Rianna J. F. de Jonker, Thierry Durroux, Henry F. Vischer, Marco Siderius, and Martine J. Smit. "Differential Involvement of ACKR3 C-Tail in β-Arrestin Recruitment, Trafficking and Internalization." Cells 10, no. 3 (March 11, 2021): 618. http://dx.doi.org/10.3390/cells10030618.

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Background: The atypical chemokine receptor 3 (ACKR3) belongs to the superfamily of G protein-coupled receptors (GPCRs). Unlike classical GPCRs, this receptor does not activate G proteins in most cell types but recruits β-arrestins upon activation. ACKR3 plays an important role in cancer and vascular diseases. As recruitment of β-arrestins is triggered by phosphorylation of the C-terminal tail of GPCRs, we studied the role of different potential phosphorylation sites within the ACKR3 C-tail to further delineate the molecular mechanism of internalization and trafficking of this GPCR. Methods: We used various bioluminescence and fluorescence resonance energy transfer-based sensors and techniques in Human Embryonic Kidney (HEK) 293T cells expressing WT or phosphorylation site mutants of ACKR3 to measure CXCL12-induced recruitment of β-arrestins and G-protein-coupled receptor kinases (GRKs), receptor internalization and trafficking. Results: Upon CXCL12 stimulation, ACKR3 recruits both β-arrestin 1 and 2 with equivalent kinetic profiles. We identified interactions with GRK2, 3 and 5, with GRK2 and 3 being important for β-arrestin recruitment. Upon activation, ACKR3 internalizes and recycles back to the cell membrane. We demonstrate that β-arrestin recruitment to the receptor is mainly determined by a single cluster of phosphorylated residues on the C-tail of ACKR3, and that residue T352 and in part S355 are important residues for β-arrestin1 recruitment. Phosphorylation of the C-tail appears essential for ligand-induced internalization and important for differential β-arrestin recruitment. GRK2 and 3 play a key role in receptor internalization. Moreover, ACKR3 can still internalize when β-arrestin recruitment is impaired or in the absence of β-arrestins, using alternative internalization pathways. Our data indicate that distinct residues within the C-tail of ACKR3 differentially regulate CXCL12-induced β-arrestin recruitment, ACKR3 trafficking and internalization.
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Nakaya, Michio, Satsuki Chikura, Kenji Watari, Natsumi Mizuno, Koji Mochinaga, Supachoke Mangmool, Satoru Koyanagi, et al. "Induction of Cardiac Fibrosis by β-Blocker in G Protein-independent and G Protein-coupled Receptor Kinase 5/β-Arrestin2-dependent Signaling Pathways." Journal of Biological Chemistry 287, no. 42 (August 10, 2012): 35669–77. http://dx.doi.org/10.1074/jbc.m112.357871.

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G-protein coupled receptors (GPCRs) have long been known as receptors that activate G protein-dependent cellular signaling pathways. In addition to the G protein-dependent pathways, recent reports have revealed that several ligands called “biased ligands” elicit G protein-independent and β-arrestin-dependent signaling through GPCRs (biased agonism). Several β-blockers are known as biased ligands. All β-blockers inhibit the binding of agonists to the β-adrenergic receptors. In addition to β-blocking action, some β-blockers are reported to induce cellular responses through G protein-independent and β-arrestin-dependent signaling pathways. However, the physiological significance induced by the β-arrestin-dependent pathway remains much to be clarified in vivo. Here, we demonstrate that metoprolol, a β1-adrenergic receptor-selective blocker, could induce cardiac fibrosis through a G protein-independent and β-arrestin2-dependent pathway. Metoprolol, a β-blocker, increased the expression of fibrotic genes responsible for cardiac fibrosis in cardiomyocytes. Furthermore, metoprolol induced the interaction between β1-adrenergic receptor and β-arrestin2, but not β-arrestin1. The interaction between β1-adrenergic receptor and β-arrestin2 by metoprolol was impaired in the G protein-coupled receptor kinase 5 (GRK5)-knockdown cells. Metoprolol-induced cardiac fibrosis led to cardiac dysfunction. However, the metoprolol-induced fibrosis and cardiac dysfunction were not evoked in β-arrestin2- or GRK5-knock-out mice. Thus, metoprolol is a biased ligand that selectively activates a G protein-independent and GRK5/β-arrestin2-dependent pathway, and induces cardiac fibrosis. This study demonstrates the physiological importance of biased agonism, and suggests that G protein-independent and β-arrestin-dependent signaling is a reason for the diversity of the effectiveness of β-blockers.
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Qu, Changxiu, Ji Young Park, Min Woo Yun, Qing-tao He, Fan Yang, Kiae Kim, Donghee Ham, et al. "Scaffolding mechanism of arrestin-2 in the cRaf/MEK1/ERK signaling cascade." Proceedings of the National Academy of Sciences 118, no. 37 (September 10, 2021): e2026491118. http://dx.doi.org/10.1073/pnas.2026491118.

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Arrestins were initially identified for their role in homologous desensitization and internalization of G protein–coupled receptors. Receptor-bound arrestins also initiate signaling by interacting with other signaling proteins. Arrestins scaffold MAPK signaling cascades, MAPK kinase kinase (MAP3K), MAPK kinase (MAP2K), and MAPK. In particular, arrestins facilitate ERK1/2 activation by scaffolding ERK1/2 (MAPK), MEK1 (MAP2K), and Raf (MAPK3). However, the structural mechanism underlying this scaffolding remains unknown. Here, we investigated the mechanism of arrestin-2 scaffolding of cRaf, MEK1, and ERK2 using hydrogen/deuterium exchange–mass spectrometry, tryptophan-induced bimane fluorescence quenching, and NMR. We found that basal and active arrestin-2 interacted with cRaf, while only active arrestin-2 interacted with MEK1 and ERK2. The ATP binding status of MEK1 or ERK2 affected arrestin-2 binding; ATP-bound MEK1 interacted with arrestin-2, whereas only empty ERK2 bound arrestin-2. Analysis of the binding interfaces suggested that the relative positions of cRaf, MEK1, and ERK2 on arrestin-2 likely facilitate sequential phosphorylation in the signal transduction cascade.
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Kumar, P., C. S. Lau, M. Mathur, P. Wang, and K. A. DeFea. "Differential effects of β-arrestins on the internalization, desensitization and ERK1/2 activation downstream of protease activated receptor-2." American Journal of Physiology-Cell Physiology 293, no. 1 (July 2007): C346—C357. http://dx.doi.org/10.1152/ajpcell.00010.2007.

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β-Arrestins-1 and 2 are known to play important roles in desensitization of membrane receptors and facilitation of signal transduction pathways. It has been previously shown that β-arrestins are required for signal termination, internalization, and ERK1/2 activation downstream of protease-activated-receptor-2 (PAR-2), but it is unclear whether they are functionally redundant or mediate specific events. Here, we demonstrate that in mouse embryonic fibroblasts (MEFs) from β-arrestin-1/2 knockout mice, Gαq signaling by PAR-2, as measured by mobilization of intracellular Ca2+, is prolonged. Only expression of β-arrestin-1 shortened the signal duration, whereas either β-arrestin-1 or 2 was able to restore PKC-induced receptor desensitization. β-arrestin-1 also mediated early, while β-arrestin-2 mediated delayed, receptor internalization and membrane-associated ERK1/2 activation. While β-arrestin-1 colocalized with a lysosomal marker (LAMP-1), β-arrestin-2 did not, suggesting a specific role for β-arrestin-1 in lysosomal receptor degradation. Together, these data suggest distinct temporal and functional roles for β-arrestins in PAR-2 signaling, desensitization, and internalization.
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Dissertations / Theses on the topic "?-arrestin"

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Sharmeen, Cynthia. "Involvement of Beta-arrestin 1 and Beta-arrestin 2 in store operated calcium entry." Mémoire, Université de Sherbrooke, 2016. http://hdl.handle.net/11143/9499.

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Résumé : La variation de la [Ca2+] intracellulaire participe à nombreux de processus biologiques. Les cellules eucaryotes expriment à la membrane plasmique une variété de canaux par lesquelles le calcium peut entrer. Dans les cellules non excitables, deux mécanismes principaux permettent l'entrée calcique; l'entrée capacitative de Ca2+ via Orai1 (SOCE) et l'entrée calcique activé par un récepteur (ROCE). Plusieurs protéines clés sont impliquées dans la régulation de ces voies d'entrée calcique, ainsi que dans l'homéostasie calcique. TRPC6 est un canal calcique impliquée dans l'entrée calcique dans les cellules à la suite d’une stimulation d’un récepteur hormonal. TRPC6 transloque à la membrane cellulaire et il y demeure jusqu'à ce que le stimulus soit retiré. Les mécanismes qui régulent le trafic et l'activation de TRPC6 sont cependant encore peu connus. Des découvertes récentes ont démontré qu'il y a un rôle potentiel de Rho kinase dans l'activité de TRPC6. Rho kinase est activée par la petite protéine G RhoA qui peut être activée par les protéines G hétérotrimériques Gα12 et Gα13. En plus de Gα12 et Gα13, les protéines de désensibilisation des GPCR β -arrestin 1 et / ou β-arrestin 2 peuvent aussi activer RhoA. Le but de notre étude est d'examiner la participation des protéines Gα12/13 et β-arrestin 1/ β-arrestin 2 dans l'activation de TRPC6 et de la protéine Orai1. Nous avons utilisé des ARN interférant (siRNA) spécifiques pour induire une réduction de l'expression de Gα12/13 ou β-arrestin 1/β-arrestin 2. La conséquence sur l’entrée de Ca2+ dans les cellules a été ensuite déterminée par imagerie calcique en temps réel suite à une stimulation par la vasopressine (AVP), thapsigargin ou carbachol. Nous avons donc identifié que dans des cellules A7r5, une lignée cellulaire de musculaires lisses vasculaires où le canal TRPC6 exprimé de manière endogène, la diminution de l’expression des protéines Gα12 ou Gα13 ne semble pas modifier l’entrée Ca2+ induit par l’AVP par rapport aux cellules témoins. D'autre part, la diminution de l’expression β-arrestin 1 ou β-arrestin 2 dans des cellules HEK 293 ainsi que des cellules HEK 293 exprimant de façon stable TRPC6 (cellules T6.11) ont augmenté l’entrée de Ca2+ induite par thapsigargin, un activateur pharmacologique de SOCE. Des études de co-immunoprécipitation démontrent une interaction entre la β-arrestin 1 et STIM1, alors qu'aucune interaction n'a été observée entre les β-arrestin 1 et Orai1. Nous avons de plus montré à l'aide d'analyse en microscopie confocale que la diminution de l’expression β-arrestin 1 ou β-arrestin 2 n’influence pas la quantité d’Orai1 à la périphérie cellulaire. Cependant, des résultats préliminaires indiquent que la diminution de l’expression β-arrestin 1 ou β-arrestin 2 augmente la quantité de STIM1-YFP dans l'espace intracellulaire et diminue sa quantité à la périphérie cellulaire. En conclusion, nous avons montré que les β-arrestin 1 ou β-arrestin 2 sont impliquées dans l'entrée capacitative de Ca2+ (SOCE) et contrôlent la quantité de STIM1 dans le réticulum endoplasmique.
Abstract : In an organism, intracellular [Ca2+] takes part in many biological processes. Eukaryotic cells express a variety of channels in the plasma membrane through which calcium can enter. In non-excitable cells, two main mechanisms allow calcium entry; the store-operated calcium entry via Orai1 (SOCE) and receptor-operated calcium entry (ROCE). Several key proteins are involved in the regulation of these calcium entry pathways as well as in calcium homeostasis. TRPC6 is a calcium channel implied in calcium entrance into the cells following hormonal stimulation and translocates to the plasma membrane. TRPC6 channel appear to the plasma membrane until the stimulus is present. Although, the mechanisms that regulate the trafficking and activation of TRPC6 are still little known. Recent findings have demonstrated that there is a potential role of Rho kinase in activity of TRPC6. Rho kinase is activated by the small G protein RhoA that itself can be activated by the heterotrimeric G proteins Gα12 and Gα13. In addition to Gα12 and Gα13 proteins, cytosolic GPCR desensitizing proteins β-arrestin 1 and/or β-arrestin 2 could also activate RhoA. The purpose of our study is to investigate the involvement of the proteins Gα12/13 and β-arrestin 1/β-arrestin 2 in the activation of TRPC6 and Orai1 protein. We used siRNA specific to Gα12/13 or β-arrestin 1/β-arrestin 2 to knockdown their endogenous expression. Then, calcium imaging in real time was performed in order to see the quantity of calcium entered into the cell following stimulation by vasopressin (AVP), thapsigargin, or carbachol. We hence identified that in A7r5 cell, vascular smooth muscle cell where TRPC6 channel expressed endogenously; reduced expression of Gα12 or Gα13 proteins does not seem to modify the AVP-induced Ca2+ entry compared to control cells. On the other hand, calcium imaging experiment in knocked down β-arrestin 1 or β-arrestin 2 in HEK 293 cells as well as HEK 293 cells stably transfected with TRPC6 (T6.11 cells) resulted in an increased thapsigargin-induced calcium entry. The co-immunoprecipitation studies demonstrate an interaction between β-arrestin 1 and STIM1, a calcium sensor in SOCE influx, while no interaction was observed between β-arrestin 1 and Orai1.We moreover showed by confocal microscopy that reduced expression of β-arrestin 1/ β-arrestin 2 does not influence the quantity of Orai1 at the cell periphery. Preliminary results showed that reduced expression of β-arrestin 1 or β-arrestin 2 increases the quantity of STIM1-YFP in the intracellular space and less it’s in peri-membrane space. In conclusion, we showed that β-arrestin 1 or β-arrestin 2 are involved in the store-operated calcium entry (SOCE) and control the quantity of STIM1 in the endoplasmic reticulum.
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Saxena, Kunal. "Arrestin interactions with the μ-opioid receptor." Thesis, University of Bristol, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.559233.

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Upon agonist binding the u-opioid receptor (MOPr) is phosphorylated and can recruit arrestin-2 (beta-arrestin-l) and arrestin-3 (p-arrestin-2). Apart from promoting the desensitization and intemalization of the MOPr, the binding of arrestins can also lead to the triggering of alternative sigvalling pathways. It has been shown that kinases including GRK2, PKC and CaMKII can regulate MOPr. Here we used GST -fusion constructs of the intracellular regions of MOPr to investigate whether arrestin-2 and -3 can bind to these sequences in vitro, and secondly to determine whether phosphorylation of these sequences by various kinases can alter their ability to bind arrestins. Arrestin-3 bound to the unphosphorylated intracellular loops (ICL2, ICL3) and the COOH-tail of the MOPr, whereas arrestin-2 displayed preferential binding to the COOH-tail. Phosphorylation of the MOPr COOH-tail by PKC and CaMKII increased arrestin-2 and -3 binding but to a lesser extent than GRK2. The full agonist DAMGO was able to increase the interaction of both GFP-arrestin-2 and -3 to the full length MOPr. Previous published work, suggests that mice lacking arrestin-3, showed reduced opiate-induced constipation and respiratory suppression and the development of tolerance to opiates such as morphine. During my masters degree at Moscow State University (Russia), I designed and synthesized small molecule inhibitors (Kt, K2 and K3; see appendix-I-Ill for the chemical structures) of the arrestin-MOPr interaction using computer-aided drug design. In the GST pull down assay, only K3 affected the arrestin-MOPr interaction. It decreased the association of arrestin-2 b~t increased the association of arrestin-3 to the COOH-tail of the MOPr. K3 did not affect the interaction of arrestin-3 with the GRK2-phosphorylated MOPr COOH-tail fusion protein. Similar results were obtained in the full length receptor, where the association of GFP- arrestin-3 with the HA-tagged-MOPr remained unaffected in the presence of K3 and DAMGO stimulation. On the other hand, in the absence of DAMGO, K3 did increase the interaction of GFP-arrestin-3 with MOPr. In addition, K3 did not bind to the MOPr orthosteric binding sites and did not affect G-protein activation in the presence and absence of DAM GO. Taken together these data suggest that even though the small molecules were unable to inhibit the arrestin-3/MOPr interaction, such a direct modulation of the arrestin-MOPr interaction is possible and specific small molecules can be designed to modulate this interaction of other GPCRs.
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3

Carter, Alison A. "Molecular pharmacology of agonist-stimulated arrestin-receptor interactions." Thesis, University of Nottingham, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.440126.

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Eidhoff, Ulf Benno. "Heterologe Expression, Kristallisation und Untersuchungen zur Struktur von Bos taurus [beta]-Arrestin-1 [Beta-Arrestin-1] und Rattus norvegicus PAR-4." [S.l. : s.n.], 2000. http://deposit.ddb.de/cgi-bin/dokserv?idn=961407883.

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5

Correll, Jennifer A. "Nicotine Sensitization in β-Arrestin 2 Knockout Adolescent Mice." Digital Commons @ East Tennessee State University, 2007. https://dc.etsu.edu/etd/2050.

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ß arrestin-2 is a protein involved in signaling of D2 receptors and plays a mediating role in sensitization to psychostimulants and the opiate morphine. In this study, 3-4 week old BA-2 KO and wild type C57/B6 mice received nicotine tartarate (s.c, 0.5 mg/kg free base) for 7 or 14 consecutive days followed by a drug-free period. An acute nicotine challenge followed the drugfree period. Results indicated that the absence of ß-arrestin-2 reduced sensitization to nicotine in Experiment 1. BA-2 KOs eventually demonstrated sensitization in Experiment 2. However, absence of ß-arrestin-2 blocked expression of sensitization on the challenge. After the challenge, brain tissue was removed and the nucleus accumbens was dissected and analyzed for brainderived neurotrophic factor (BDNF). Results showed that BDNF positively correlated with behavioral results. These results appear to indicate the importance of the ß-arrestin-2 protein in locomotor sensitization and that dopamine signaling is related to BDNF.
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Lally, Ciara. "Structural and functional characterization of the arrestin-rhodopsin complex." Doctoral thesis, Humboldt-Universität zu Berlin, 2017. http://dx.doi.org/10.18452/18570.

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Die Aufgabe des Proteins Arrestin ist die Beendigung der Signalweitergabe über den GPCR Signalweg. In Stäbchenzellen bindet Arrestin an Licht-aktiviertes phosphoriliertes Rhodopsin um die Signalweitergabe zu unterdrücken. Die Bindung von Arrestin an Rhodopsin erfolgt in zwei Schritten. Zunächst wechselwirkt Arrestin mit dem phosphorilierten C-Terminus von Rhodopsin und bildet einen prä-Komplex, dies induziert Konformationsänderungen im Arrestin wodurch die Bildung eines High-affinity Komplex unter Kopplung an den helikalen Kern des aktivierten Rezeptors erfolgen kann. Biochemische Untersuchungen und Kristallstrukturen haben einen Einblick in die Konformation des Komplexes aus Arrestin und Rhodopsin ermöglicht. In dieser Arbeit werden site-directed Fluorezenz Experimente angewandt um die strukturellen Änderungen zu untersuchen, die bei der Bindung von Arrestin an Rhodopsin ablaufen und der nterschiedlichen Bindungsmodi innerhalb der Wechselwirkung zwischen Arrestin und Rhodopsin. Insbesondere wird hier eine, bisher nicht beschriebene, Assoziation von Arrestin an die Membran untersucht. Des Weiteren wurden Erkenntnisse über die Struktur des prä-Komplexes gewonnen. Die Konformation vom Arrestin im prä-Komplex scheint die Konformation im Basalzustand nachzubilden unter Beteiligung zweier Kontaktstellen: Interaktion mit dem phosphorilierten C-Terminus des Rezeptors und Assoziation mit der Membran. Beim Übergang in den High-affinity Komplex durchläuft Arrestin eine Konformationsänderung in eine aktivere Konformation: der C-Terminus wird verdrängt, es erfolgt eine Neuausrichtung der zentralen flexiblen Schleifen und die Orientierung des Membranankers ändert sich. Die Aufgabe des prä-Komplexes ist somit Arrestin und den Rezeptor zusammen zu bringen sowie die korrekte Orientierung sicherzustellen um einen schnellen Übergang in den High-affinity Komplex zu ermöglichen.
The protein arrestin is responsible for termination of GPCR signalling. In the rod cell, arrestin binds light-activated phosphorylated rhodopsin in order to block further signal transduction. The binding of arrestin to rhodopsin is a two-step process. Arrestin first interacts with the phosphorylated receptor C-terminus in a pre-complex, which induces conformational changes in arrestin that allow coupling to the helical core of the active receptor in a high-affinity complex. Biochemical studies and crystal structures have provided insights into the conformation of the arrestin-rhodopsin complex. This dissertation describes site-directed fluorescence experiments, which were carried out to further investigate the conformational changes occurring upon arrestin binding to rhodopsin and the nature of different binding modes of the arrestin-rhodopsin interaction. In particular this involved characterization of a previously unidentified association of arrestin with the membrane, as well as further elucidation of the structure of the pre-complex. The conformation of arrestin in the pre-complex is indicated to resemble that of the basal state of arrestin, and involves two sites of contact: interaction with the phosphorylated receptor C-terminus, and association with the membrane. Upon transition to the high-affinity complex, arrestin undergoes a conformational change to a more active conformation: the auto-inhibitory C-tail is displaced, there is movement within the central flexible loops, and the orientation of the membrane anchor changes. The pre-complex therefore most likely functions to bring arrestin and the receptor into close contact, and in the correct orientation, to allow for fast transition to the high-affinity complex.
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Obeid, Joëlle. "Caractérisation de la fonction des β-arrestines dans les cellules β pancréatiques : recherche de nouvelles stratégies thérapeutiques pour le diabète de type 2." Thesis, Montpellier, 2018. http://www.theses.fr/2018MONTT066.

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Les pertes de la fonction et de la masse des cellules beta pancréatiques jouent un rôle central dans le diabète de type 2 (DT2). Les beta-arrestines 1 et 2 (ARRB1 et ARRB2), sont impliquées dans la sécrétion et/ou la survie des cellules beta pancréatiques.Dans une première étude, afin de caractériser précisément la fonction d’ARRB1 dans les cellules beta pancréatiques, nous avons eu pour objectif de générer des souris invalidées spécifiquement dans ces cellules en utilisant le système Cre/lox sous le contrôle du promoteur Ins1. Des études avaient été publiées à partir des deux lignées Ins1Cre-/+ et Arrb1f/f. Nous avons généré et travaillé sur les souris Arrb1f/f :Ins1Cre-/+. Le phénotype des souris Arrb1f/f :Ins1Cre-/+ était faible et surtout non reproductible comparé aux souris Arrb1f/f :Ins1Cre-/- utilisées comme témoins. Le faible niveau d’expression d'Arrb1 dans les cellules beta et le manque d'anticorps spécifique pour l'immunocytochimie ont rendu difficile la vérification de l'absence d'expression de ARRB1 dans ces cellules. Après séquençage du gène modifié Arrb1 des souris “floxées“, nous avons pu montrer que l'insertion du premier site loxP avait induit un décalage du cadre de lecture introduisant un codon stop et, par conséquent, la non-expression du gène Arrb1. Étant donné que les souris Arrb1 “floxées“ utilisées comme témoins étaient déjà knockout (KO), le projet utilisant ces souris a dû être arrêté.Notre équipe a rapporté l'implication d'ARRB2 dans la régulation de la masse des cellules bêta pancréatique, mais son rôle dans la signalisation du récepteur du Glucagon-Like Peptide-1 (GLP-1R), une cible thérapeutique majeure du DT2, n'avait pas encore été exploré.Nous avons montré, dans une deuxième étude, une meilleure tolérance orale au glucose ainsi qu’une augmentation de la sécrétion d’insuline chez les souris Arrb2 KO par rapport aux souris témoins sur les îlots en présence des concentrations physiologiques circulantes de GLP-1. Ceci est corrélé à une production d’AMPc et un recrutement de la PKA plus élevés dans les cellules beta Arrb2 KO. A l’inverse, l’activation des kinases ERK1/2 est diminuée indiquant un recrutement majeur des ERK1/2 par ARRB2 au GLP-1R. En parallèle, j’ai montré que les taux de ARRB1 et ARRB2 des îlots pancréatiques sont altérés par des conditions diabétogènes et diabétiques. Mes résultats démontrent clairement un rôle critique de ARRB2 dans la signalisation du GLP-1R. Un défaut d’expression de la protéine pourrait participer au déficit des mécanismes de compensation de la masse fonctionnelle des cellules beta conduisant au DT2
The loss of function and mass of pancreatic beta-cells play a central role in type 2 diabetes (T2D). Beta-arrestin 1 and 2 (ARRB1 and ARRB2) are involved in insulin secretion and/or beta-cell survival. In a first study, in order to characterize the role of ARRB1 in beta-cells, we aimed to invalidate the Arrb1 gene specifically in these cells using the Cre/lox system under the control of the Ins1 promoter. Studies had been published with both Ins1Cre-/+ and Arrb1f/f lines. We generated Arrb1f/f:Ins1Cre-/+ mice. The phenotype of Arrb1f/f :Ins1Cre-/+ mice was weak with a lack of reproducibility compared to Arrb1f/f :Ins1Cre-/- mice used as controls. The low expression level of Arrb1 in beta-cells and the lack of specific antibody for immunocytochemistry made it difficult to verify the absence of expression of ARRB1 in these cells. After sequencing the modified Arrb1 gene of the “floxed” mice, we observed that the insertion of the first loxP site induced a shift in the reading frame introducing a stop codon and, consequently, the non-expression of the Arrb1 gene. Since the “floxed“ Arrb1 mice used as controls were already knockout (KO), the project using these mice was stopped.Our team has reported the involvement of ARRB2 in the regulation of beta-cell mass, but its role in Glucagon-Like Peptide-1 (GLP-1) receptor signaling, a major therapeutic target for T2D, remained to be explored. In a second study, we showed a better glucose tolerance and an increase in insulin secretion from isolated islets in Arrb2KO compared to control mice in the presence of physiological circulating concentrations of GLP-1. This was correlated with higher cAMP production and PKA activation in Arrb2KO beta-cells. By contrast, the activation of ERK1/2 kinases was decreased indicating a major recruitment of ERK1/2 by ARRB2 to GLP-1R. In parallel, we showed that the expression levels of ARRB1 and ARRB2 in pancreatic islets were altered in diabetogenic and diabetic conditions. My results clearly demonstrate a critical role of ARRB2 in GLP-1R singaling which could impact the function, maintenance and plasticity of beta-cell mass in response to GLP-1. A lack of expression of ARRB2 could participate in the deficit of compensatory mechanisms of the functional beta-cell mass leading to T2D
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Puca, Loredana. "Role of the arrestin family in notch pathway in mammals." Paris 6, 2013. http://www.theses.fr/2013PA066350.

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La voie de signalisation Notch est une voie conservée au cours de l’évolution impliquée dans le développement embryonnaire et dans l'homéostasie tissuetaire chez les adultes. Un certain nombre de modifications post-traductionnelles ont été impliquées dans la régulation de l'activité du récepteur Notch et certaines d'entre elles ont une incidence sur la dégradation du récepteur Notch non activé. Le point de départ de mon projet de thèse est la découverte chez la Drosophile montrant que la protéine adaptateur Kurtz, l'unique arrestine non-visuelle de la Drosophile, est un régulateur essentiel de la voie de signalisation Notch. Chez les mammifères, la famille des arrestines (à l'exclusion des arrestines visuelles) est composée de deux sous-familles: β-arrestines et α-arrestines. Les principaux résultats que j'ai obtenus montrent que les deux arrestines α-β sont recrutées par le récepteur Notch non-activé et permettent l’ubiquitination de Notch médiée par Itch chez les mammifères. Une hétérodimérisation entre une β-arrestine et l’ α-arrestine ARRDC1 est nécessaire pour promouvoir l'ubiquitination de Notch et la dégradation du récepteur Notch non activé dans le lysosome. Pour conclure, nous montrons pour la première fois que α et β-arrestines agissent comme des régulateurs négatifs de la signalisation Notch, mettant en évidence l'existence d'une coopération entre ces protéines adaptatrices pour réguler le trafic des récepteurs
Notch signaling is an evolutionary conserved pathway implicated in embryonic development and in adult tissue homeostasis. A number of post-translational modifications have been implicated in regulating the activity of Notch receptor and some of them affect the degradation of non-activated Notch receptor. The starting points of my PhD project are Drosophila findings showing that the adaptor protein Kurtz, the unique non-visual arrestin in Drosophila, is an essential regulator of Notch signaling. In mammals the arrestin family (excluding the visual arrestins) is composed of two sub-families: -arrestins and-arrestins. The main results that I have obtained show that both -arrestins and -arrestins are recruited to non-activated Notch receptor and allow Itch-mediated Notch ubiquitination in mammals. Biochemical evidence shows that an heterodimerization between -arrestins and the -arrestin ARRDC1 is required to promote Notch ubiquitination and its lysosomal degradation. To conclude, we show for the first time that the --arrestin heterodimer is functionally involved in the degradation of Notch receptor, highlighting the existence of a cooperation between these adaptor proteins to regulate receptor trafficking
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Celver, Jeremy Phillip. "Molecular mechanisms of opioid receptor regulation by GRK and arrestin /." Thesis, Connect to this title online; UW restricted, 2002. http://hdl.handle.net/1773/6299.

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Armando, Sylvain. "Structure quaternaire des récepteurs de chimiokines CXCR4 et CCR2 et interaction avec leur effecteurs." Thesis, Montpellier 2, 2010. http://www.theses.fr/2010MON20208/document.

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Les récepteurs couplés aux protéines G (RCPG) sont la famille de récepteurs membranaires la plus représentée chez les vertébrés, et la plus grande cible thérapeutique chez l'Homme. L'évolution du paradigme initial qui énonçait une stœchiométrie récepteur : protéine G : effecteur de 1 :1 :1 sera présentée sur le modèle des récepteurs aux chimiokines CXCR4 et CCR2. Grâce à la technique de transfert d'énergie par bioluminescence (BRET), les travaux réalisés durant cette thèse montrent (1) que c'est par un couplage alternatif de CXCR4 à Gα13 au lieu de la voie classique Gαi que les cellules de cancer du sein migrent pour former des métastases, (2) que la désensibilisation de CXCR4 implique le recrutement d'une combinaison définie de protéines (GRK et arrestines) permettant l'arrêt sélectif des multiples voies engagées en réponse à l'agoniste, et (3) que le protomère CXCR4 a un rôle déterminant dans l'engagement de la protéine Gαi et le recrutement de la β-arrestine par l'hétéro-oligomère CXCR4/CCR2 lorsque CCR2 est activé. Dans cette dernière et principale étude, les résultats montrent également que le dimère CCR2 peut s' assembler au dimère CXCR4 pour former un tétramère, et que l'activation de CCR2 influence la conformation du dimère CXCR4. Les phénomènes de coopérativité et d'activation asymétrique déjà rapportés pour cet hétérodimère pourraient donc impliquer l'interaction de quatre protomères. En conclusion les travaux effectués durant cette thèse démontrent une régulation supplémentaire de l'activité des récepteurs chimiokines au niveau de leur structure quaternaire, de leur signalisation, et de l'arrêt de cette signalisation
G protein coupled receptors (GPCR) are the most represented cell surface receptors among vertebrates, and the major therapeutic target in humans. The initial paradigm stating a 1 :1 :1 stoichiometry for receptor :G protein :effector has evolved to a more complex model, as illustrated here with the example of the chemokine receptors CXCR4 and CCR2. Bioluminescence resonance energy transfer (BRET) was used to demonstrate that (1) CXCR4 is able to couple Gα13 instead of Gαi to promote breast cancer metastasis, (2) the multiple pathways engaged by stimulation of CXCR4 are selectively desensitized by the specific recruitment of a defined combination of proteins (GRKs and arrestins) and (3) the CXCR4 protomer plays a crucial role during Gαi engagement and β-arrestin recruitment by the CXCR4/CCR2 heterodimer upon CCR2 activation. In this last and main study, the results shown also demonstrate that CCR2 dimers could assemble with CX CR4 dimers into hetero-tetramers, and that CCR2 activation leads to a conformational change in the CXCR4 dimer. Former results showing cooperativity and asymmetric activation of a simple CXCR4/CCR2 heterodimer could then be applied to a tetramer. To conclude, the work done during this thesis demonstrates a more sophisticated regulation of chemokine receptors than previously suspected at 3 different levels: quaternary structure of the protomers, G protein signalling, and signalling termination
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Books on the topic "?-arrestin"

1

Gurevich, Vsevolod V., ed. The Structural Basis of Arrestin Functions. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-57553-7.

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Scott, Mark G. H., and Stéphane A. Laporte, eds. Beta-Arrestins. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9158-7.

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Parker, Brenda. Arresting love. Anstey: Thorpe, 1991.

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Luke, Allyn. Contaminant arresting systems. Trenton, NJ: New Jersey Dept. of Transportation, 2002.

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Dijk, W. A. M. van., Hovens J. L, and Netherlands Koninklijke Marechaussee, eds. Arresting war criminals. Nijmegen: Wolf Legal Productions, 2001.

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Traldi, Andrea. Gli arresti domiciliari. Roma: Ianua, 1988.

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Upadhyay, Samrat. Arresting God in Kathmandu. New Delhi: Rupa & Co., 2002.

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Joint Commission on Accreditation of Healthcare Organizations., ed. Tuberculosis: Arresting everyone's enemy. 2nd ed. Oakbrook Terrace, IL: Joint Commission Resources, 2007.

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Arresting God in Kathmandu. Boston: Houghton Mifflin, 2001.

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Joint Commission on Accreditation of Healthcare Organizations., ed. Tuberculosis: Arresting everyone's enemy. Oakbrook Terrace, IL: Joint Commission on Accreditation of Healthcare Organizations, 1996.

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Book chapters on the topic "?-arrestin"

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Craft, Cheryl Mae, and Janise D. Deming. "Cone Arrestin: Deciphering the Structure and Functions of Arrestin 4 in Vision." In Arrestins - Pharmacology and Therapeutic Potential, 117–31. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-41199-1_6.

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Willis, Miranda J., and George S. Baillie. "Arrestin-Dependent Localization of Phosphodiesterases." In Arrestins - Pharmacology and Therapeutic Potential, 293–307. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-41199-1_15.

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Cameron, Ryan T., and George S. Baillie. "Arrestin Regulation of Small GTPases." In Arrestins - Pharmacology and Therapeutic Potential, 375–85. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-41199-1_19.

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Kenakin, Terry. "Quantifying Biased β-Arrestin Signaling." In Arrestins - Pharmacology and Therapeutic Potential, 57–83. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-41199-1_3.

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Zhao, Yang, and Kunhong Xiao. "Proteomic Analysis of the β-Arrestin Interactomes." In Beta-Arrestins, 217–32. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9158-7_14.

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Strungs, Erik G., Louis M. Luttrell, and Mi-Hye Lee. "Probing Arrestin Function Using Intramolecular FlAsH-BRET Biosensors." In Beta-Arrestins, 309–22. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9158-7_19.

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Chen, Qiuyan, Ya Zhuo, Miyeon Kim, Susan M. Hanson, Derek J. Francis, Sergey A. Vishnivetskiy, Christian Altenbach, Candice S. Klug, Wayne L. Hubbell, and Vsevolod V. Gurevich. "Self-Association of Arrestin Family Members." In Arrestins - Pharmacology and Therapeutic Potential, 205–23. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-41199-1_11.

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Lally, Ciara C. M., and Martha E. Sommer. "Quantification of Arrestin–Rhodopsin Binding Stoichiometry." In Methods in Molecular Biology, 235–50. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2330-4_16.

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Yvinec, Romain, Mohammed Akli Ayoub, Francesco De Pascali, Pascale Crépieux, Eric Reiter, and Anne Poupon. "Workflow Description to Dynamically Model β-Arrestin Signaling Networks." In Beta-Arrestins, 195–215. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9158-7_13.

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Luan, Bing, Jian Zhao, and Gang Pei. "Methods to Investigate β-Arrestin Function in Metabolic Regulation." In Beta-Arrestins, 365–84. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9158-7_23.

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Conference papers on the topic "?-arrestin"

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Akins-Rivers, E. Joy, Nikia Smith, and Ricardo M. Richardson. "Abstract B46: Investigating the role of β-arrestin-2 in prostate cancer disparity using a β-arrestin-2 deficient mouse model of prostate cancer." In Abstracts: AACR International Conference on the Science of Cancer Health Disparities‐‐ Sep 18-Sep 21, 2011; Washington, DC. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1055-9965.disp-11-b46.

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Lin, Rui, David A. Zidar, and Julia K. L. Walker. "Beta-arrestin-2-dependent Signaling Promotes Th2 Cell CCR4-mediated Chemotaxis." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a4049.

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Sobolesky, Philip M., Tanyau Zhou, Arielle Gorstein, Julie A. Woolworth, and Omar Moussa. "Abstract 4070: β-arrestin-2 mediated regulation of plasminogen activator inhibitor Type 1." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-4070.

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Pillai, Smitha R., Michael Damit, and Srikumar Chellappan. "Abstract 2951: Nicotine induced EMT involves β-arrestin-1 mediated regulation of E2F1 target genes." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-2951.

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Masannat, Jude, Yushan Zhang, Hamsa Purayil, Iqbal Mahmud, and Yehia Daaka. "Abstract 1982: β-arrestin 2 mediates tumor growth and metastasis in renal cell carcinoma cells." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-1982.

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Pillai, Smitha, Jose Trevino, Bhupendra Rawal, Sandeep Singh, Xueli Li, Michael Schell, Eric Haura, Gerold Bepler, and Srikumar Chellappan. "Abstract 4993: Nicotine induced EMT and metastasis of human NSCLC : Role of beta-arrestin-1." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-4993.

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Pera, T., E. Tompkins, D. A. Deshpande, A. P. Nayak, and R. B. Penn. "Biased Regulation of OGR1 Biased Signaling in Airway Smooth Muscle Cells: GRK2/3 and Arrestin Potluck." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a2849.

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Mowart, Tonelia A., Timothy Adekoya, Nikia Smith, Tonya S. Lane, and Ricardo M. Richardson. "Abstract B005: Ginger consumption inhibits β-arrestin-2 expression and functions in melanoma and prostate cancer cells." In Abstracts: AACR Special Conference: Prostate Cancer: Advances in Basic, Translational, and Clinical Research; December 2-5, 2017; Orlando, Florida. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.prca2017-b005.

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Kallifatidis, Georgios, Daniel Munoz, Rajendra K. Singh, and Bal L. Lokeshwar. "Abstract 4993: β-arrestin-2 regulates CXCR7-mediated EGFR transactivation and tumor cell proliferation in prostate cancer cells." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-4993.

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Johnston, R. A., A. W. Pilkington, IV, M. L. Kashon, and J. S. Reynolds. "β-Arrestin-1 Deficiency Reduces Airway Responsiveness to Methacholine in a Mouse Model of Irritant-Induced Occupational Asthma." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a4508.

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Reports on the topic "?-arrestin"

1

Civale, L., L. Krusin-Elbaum, A. D. Marwick, F. Holtzberg, C. Feild, J. R. Thompson, R. Wheeler, M. A. Kirk, and Y. R. Sun. Arresting vortex motion in YBaCuO crystals with splay in columnar defects. Office of Scientific and Technical Information (OSTI), January 1994. http://dx.doi.org/10.2172/204571.

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Clague, J. J., and S. G. Evans. A self-arresting moraine dam failure, St. Elias Mountains, British Columbia. Natural Resources Canada/ESS/Scientific and Technical Publishing Services, 1992. http://dx.doi.org/10.4095/132803.

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Wagener, Brant M. The Role of CXCR4 and Arrestins in Breast Cancer Signaling and Apoptosis. Fort Belvoir, VA: Defense Technical Information Center, February 2006. http://dx.doi.org/10.21236/ada448129.

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Wagener, Brant M. The Role of CXCR4 and Arrestins in Breast Cancer Signaling and Apoptosis. Fort Belvoir, VA: Defense Technical Information Center, February 2005. http://dx.doi.org/10.21236/ada434113.

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Carlson, Mark, Kris James Mitchener, and Gary Richardson. Arresting Banking Panics: Fed Liquidity Provision and the Forgotten Panic of 1929. Cambridge, MA: National Bureau of Economic Research, October 2010. http://dx.doi.org/10.3386/w16460.

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Bly, Peter. Development of expedient ultra-high molecular weight aircraft arresting system panel installation procedures. Engineer Research and Development Center (U.S.), July 2020. http://dx.doi.org/10.21079/11681/37536.

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Brown, E. R. Evaluation of Ultra High Molecular Weight (UHMW) Polyethylene Panels for Aircraft Arresting Systems. Fort Belvoir, VA: Defense Technical Information Center, August 2009. http://dx.doi.org/10.21236/ada508608.

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Gervasio, Dominic. Sensing and arresting metal corrosion in molten chloride salts at 800 degrees Celsius. Office of Scientific and Technical Information (OSTI), July 2021. http://dx.doi.org/10.2172/1806305.

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Prud’homme, Joseph. Quakerism, Christian Tradition, and Secular Misconceptions: A Christian’s Thoughts on the Political Philosophy of Ihsan. IIIT, October 2020. http://dx.doi.org/10.47816/01.006.20.

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Abstract:
In his elegant and insightful book Muqtedar Khan admonishes Muslims to do beautiful things. It is an arresting call in a book itself beautiful in style, clarity, and boldness of vision for a better world. Professor Khan’s quest for beauty in a specific Muslim context: the beauty that arises when actions are done with the inescapable sense that God sees all one does – or, Ihsan. But what exactly do the commands of God require of those who, knowing He is watching, set themselves the task of scrupulously doing His will?
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10

Sparacino, PeterL, Joseph W. Krulikowski, and John F. Kenefick. The National Shipbuilding Research Program, 1990 Ship Production Symposium, Paper No. 7B-2: Photogrammetry, Shipcheck of USS Constellation (cv64) Arresting Gear Engines. Fort Belvoir, VA: Defense Technical Information Center, August 1990. http://dx.doi.org/10.21236/ada451794.

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