Relevant bibliographies by topics / Arrestin Proteins

Academic literature on the topic 'Arrestin Proteins'

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Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Arrestin Proteins"

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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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Becuwe, Michel, Antonio Herrador, Rosine Haguenauer-Tsapis, Olivier Vincent, and Sébastien Léon. "Ubiquitin-Mediated Regulation of Endocytosis by Proteins of the Arrestin Family." Biochemistry Research International 2012 (2012): 1–12. http://dx.doi.org/10.1155/2012/242764.

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In metazoans, proteins of the arrestin family are key players of G-protein-coupled receptors (GPCRS) signaling and trafficking. Following stimulation, activated receptors are phosphorylated, thus allowing the binding of arrestins and hence an “arrest” of receptor signaling. Arrestins act by uncoupling receptors from G proteins and contribute to the recruitment of endocytic proteins, such as clathrin, to direct receptor trafficking into the endocytic pathway. Arrestins also serve as adaptor proteins by promoting the recruitment of ubiquitin ligases and participate in the agonist-induced ubiquitylation of receptors, known to have impact on their subcellular localization and stability. Recently, the arrestin family has expanded following the discovery of arrestin-related proteins in other eukaryotes such as yeasts or fungi. Surprisingly, most of these proteins are also involved in the ubiquitylation and endocytosis of plasma membrane proteins, thus suggesting that the role of arrestins as ubiquitin ligase adaptors is at the core of these proteins' functions. Importantly, arrestins are themselves ubiquitylated, and this modification is crucial for their function. In this paper, we discuss recent data on the intricate connections between arrestins and the ubiquitin pathway in the control of endocytosis.
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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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Spillmann, Martin, Larissa Thurner, Nina Romantini, Mirjam Zimmermann, Benoit Meger, Martin Behe, Maria Waldhoer, Gebhard F. X. Schertler, and Philipp Berger. "New Insights into Arrestin Recruitment to GPCRs." International Journal of Molecular Sciences 21, no. 14 (July 13, 2020): 4949. http://dx.doi.org/10.3390/ijms21144949.

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G protein-coupled receptors (GPCRs) are cellular master regulators that translate extracellular stimuli such as light, small molecules or peptides into a cellular response. Upon ligand binding, they bind intracellular proteins such as G proteins or arrestins, modulating intracellular signaling cascades. Here, we use a protein-fragment complementation approach based on nanoluciferase (split luciferase assay) to assess interaction of all four known human arrestins with four different GPCRs (two class A and two class B receptors) in live cells. Besides directly tagging the 11S split-luciferase subunit to the receptor, we also could demonstrate that membrane localization of the 11S subunit with a CAAX-tag allowed us to probe arrestin recruitment by endogenously expressed GPCRs. Varying the expression levels of our reporter constructs changed the dynamic behavior of our assay, which we addressed with an advanced baculovirus-based multigene expression system. Our detection assay allowed us to probe the relevance of each of the two arrestin binding sites in the different GPCRs for arrestin binding. We observed remarkable differences between the roles of each arresting binding site in the tested GPCRs and propose that the distinct advantages of our system for probing receptor interaction with effector proteins will help elucidate the molecular basis of GPCR signaling efficacy and specificity in different cell types.
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Wess, Jürgen. "The Two β-Arrestins Regulate Distinct Metabolic Processes: Studies with Novel Mutant Mouse Models." International Journal of Molecular Sciences 23, no. 1 (January 2, 2022): 495. http://dx.doi.org/10.3390/ijms23010495.

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The two β-arrestins (β-arrestin-1 and -2; alternative names: arrestin-2 and -3, respectively) are well known for their ability to inhibit signaling via G protein-coupled receptors. However, β-arrestins can also act as signaling molecules in their own right. Although the two proteins share a high degree of sequence and structural homology, early studies with cultured cells indicated that β-arrestin-1 and -2 are not functionally redundant. Recently, the in vivo metabolic roles of the two β-arrestins have been studied using mutant mice selectively lacking either β-arrestin-1 or -2 in cell types that are of particular relevance for regulating glucose and energy homeostasis. These studies demonstrated that the β-arrestin-1 and -2 mutant mice displayed distinct metabolic phenotypes in vivo, providing further evidence for the functional heterogeneity of these two highly versatile signaling proteins.
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Gurevich, Vsevolod V., and Eugenia V. Gurevich. "Solo vs Chorus: Monomers and Oligomers of Arrestin Proteins." International Journal of Molecular Sciences 23, no. 13 (June 29, 2022): 7253. http://dx.doi.org/10.3390/ijms23137253.

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Three out of four subtypes of arrestin proteins expressed in mammals self-associate, each forming oligomers of a distinct kind. Monomers and oligomers have different subcellular localization and distinct biological functions. Here we summarize existing evidence regarding arrestin oligomerization and discuss specific functions of monomeric and oligomeric forms, although too few of the latter are known. The data on arrestins highlight biological importance of oligomerization of signaling proteins. Distinct modes of oligomerization might be an important contributing factor to the functional differences among highly homologous members of the arrestin protein family.
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Vishnivetskiy, Sergey A., Luis E. Gimenez, Derek J. Francis, Susan M. Hanson, Wayne L. Hubbell, Candice S. Klug, and Vsevolod V. Gurevich. "Few Residues within an Extensive Binding Interface Drive Receptor Interaction and Determine the Specificity of Arrestin Proteins." Journal of Biological Chemistry 286, no. 27 (April 6, 2011): 24288–99. http://dx.doi.org/10.1074/jbc.m110.213835.

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Arrestins bind active phosphorylated forms of G protein-coupled receptors, terminating G protein activation, orchestrating receptor trafficking, and redirecting signaling to alternative pathways. Visual arrestin-1 preferentially binds rhodopsin, whereas the two non-visual arrestins interact with hundreds of G protein-coupled receptor subtypes. Here we show that an extensive surface on the concave side of both arrestin-2 domains is involved in receptor binding. We also identified a small number of residues on the receptor binding surface of the N- and C-domains that largely determine the receptor specificity of arrestins. We show that alanine substitution of these residues blocks the binding of arrestin-1 to rhodopsin in vitro and of arrestin-2 and -3 to β2-adrenergic, M2 muscarinic cholinergic, and D2 dopamine receptors in intact cells, suggesting that these elements critically contribute to the energy of the interaction. Thus, in contrast to arrestin-1, where direct phosphate binding is crucial, the interaction of non-visual arrestins with their cognate receptors depends to a lesser extent on phosphate binding and more on the binding to non-phosphorylated receptor elements.
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Zbieralski, Kacper, and Donata Wawrzycka. "α-Arrestins and Their Functions: From Yeast to Human Health." International Journal of Molecular Sciences 23, no. 9 (April 30, 2022): 4988. http://dx.doi.org/10.3390/ijms23094988.

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α-Arrestins, also called arrestin-related trafficking adaptors (ARTs), constitute a large family of proteins conserved from yeast to humans. Despite their evolutionary precedence over their extensively studied relatives of the β-arrestin family, α-arrestins have been discovered relatively recently, and thus their properties are mostly unexplored. The predominant function of α-arrestins is the selective identification of membrane proteins for ubiquitination and degradation, which is an important element in maintaining membrane protein homeostasis as well as global cellular metabolisms. Among members of the arrestin clan, only α-arrestins possess PY motifs that allow canonical binding to WW domains of Rsp5/NEDD4 ubiquitin ligases and the subsequent ubiquitination of membrane proteins leading to their vacuolar/lysosomal degradation. The molecular mechanisms of the selective substrate’s targeting, function, and regulation of α-arrestins in response to different stimuli remain incompletely understood. Several functions of α-arrestins in animal models have been recently characterized, including redox homeostasis regulation, innate immune response regulation, and tumor suppression. However, the molecular mechanisms of α-arrestin regulation and substrate interactions are mainly based on observations from the yeast Saccharomyces cerevisiae model. Nonetheless, α-arrestins have been implicated in health disorders such as diabetes, cardiovascular diseases, neurodegenerative disorders, and tumor progression, placing them in the group of potential therapeutic targets.
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Seyedabadi, Mohammad, Mehdi Gharghabi, Eugenia V. Gurevich, and Vsevolod V. Gurevich. "Receptor-Arrestin Interactions: The GPCR Perspective." Biomolecules 11, no. 2 (February 4, 2021): 218. http://dx.doi.org/10.3390/biom11020218.

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Arrestins are a small family of four proteins in most vertebrates that bind hundreds of different G protein-coupled receptors (GPCRs). Arrestin binding to a GPCR has at least three functions: precluding further receptor coupling to G proteins, facilitating receptor internalization, and initiating distinct arrestin-mediated signaling. The molecular mechanism of arrestin–GPCR interactions has been extensively studied and discussed from the “arrestin perspective”, focusing on the roles of arrestin elements in receptor binding. Here, we discuss this phenomenon from the “receptor perspective”, focusing on the receptor elements involved in arrestin binding and emphasizing existing gaps in our knowledge that need to be filled. It is vitally important to understand the role of receptor elements in arrestin activation and how the interaction of each of these elements with arrestin contributes to the latter’s transition to the high-affinity binding state. A more precise knowledge of the molecular mechanisms of arrestin activation is needed to enable the construction of arrestin mutants with desired functional characteristics.
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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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Dissertations / Theses on the topic "Arrestin Proteins"

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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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Wilham, Laura Elizabeth. "The role of [beta]-arrestin in agonist-induced down-regulation of the M₁mAChR." CONNECT TO THIS TITLE ONLINE, 2006. http://etd.lib.umt.edu/theses/available/etd-03022007-104437/.

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Parisis, Nikolaos. "Identification of PAR-2-regulated ERK substrates and (Beta)-arrestin-interacting proteins in invasive breast cancer cells." Thesis, University of Essex, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.520107.

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Bengreed, Amal H. I. "Characterisation of P2Y receptor-mediated contractile signalling and its regulation by G protein coupled receptor kinases and arrestin proteins in a rat bladder smooth muscle." Thesis, University of Leicester, 2018. http://hdl.handle.net/2381/42795.

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ATP released from parasympathetic nerves can mediated bladder contraction, can activate purinergic P2Y/Gq/11-coupled G protein-coupled receptors (GPCR) expressed on detrusor (bladder) smooth muscle cells (DSMC). P2Y/Gq/11 signalling activates phospholipase C (PLC) and increases intracellular calcium concentrations to induce contraction. DSMC contractile GPCR activity is tightly regulated to prevent inappropriate contraction/incontinence. Additionally, GPCRs activity is regulated by G protein-coupled receptor kinase (GRK) and arrestin proteins, it is likely that they play a similar role in DSMC, and may help to maintain continence. Combining confocal imaging, calcium-sensitive dyes and selective P2X and P2Y receptor agonists/antagonists, showed that after 3-4 days in culture DSMC calcium signals were mediated by P2Y1 and P2Y2, but not P2X, P2Y4 or P2Y6 receptors. Repeated agonist additions indicated a desensitization of P2Y1 and P2Y2 activated phospholipase C (PLC)/Ca2+ signals, which was restored when the washout period between agonist challenges was increased. Transfection of DSMC with dominant-negative, catalytically inactive GRK mutants, which block endogenous GRK function, showed that P2Y1 and P2Y2 receptor stimulated calcium signalling was selectively regulated by GRK3 and GRK2, respectively. Furthermore, desensitization of P2Y1 and P2Y2 receptor PLC/Ca2+ was attenuated following RNAi-mediated knockdown of arrestin2 or arrestin3, suggesting both arrestins were able to regulate P2Y1/2 receptor signalling. To mimic the effects of obstructive bladder, DSMC were mechanically stretched which resulted in increased GRK2, and decreased GRK3/5/6 expression. These data show that DSMC express functional P2Y1/P2Y2 receptors which mediate purinergic agonist PLC/Ca2+ signalling, implying roles for P2Y1 and P2Y2 in bladder contraction and voiding. Furthermore, P2Y1 and P2Y2 receptor are selectively regulated by GRK and arrestin proteins, which suggests that GRK and arrestin proteins play an important role in the regulation of bladder tone. Furthermore, since GRK expression following mechanical stretch this may in turn affect GPCR signalling and produce dysregulation of DSMC contraction observed during incontinence.
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Davidson, Reshma. "Regulation of Septum Formation by Two Novel Proteins Art1 and Bga1 in Fission Yeast Cytokinesis." The Ohio State University, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=osu1469185292.

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Fessart, Delphine. "Regulation of the endocytic adaptor proteins [beta] arrestin and AP-2 during clathrin-mediated internalization of Angiotensin II type 1 receptor." Thesis, McGill University, 2006. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=102501.

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G protein-coupled receptors (GPCRs) are the largest family of cell-surface receptors. They transduce the signals mediated by a diverse range of signalling molecules, including ions, amines, and peptides, as well as photons, to mediate intracellular functions. These receptors play a fundamental role in many physiological responses such as cardiovascular functions. To remain responsive to their environment, cells must find a way to rapidly desensitize and resensitize their activated GPCRs. Desensitization of receptors, for instance, involves the phosphorylation of receptors by G protein-coupled receptor kinase (GRKs) followed by the recruitment of betaarrestin. This interferes with the binding of the G protein (the signalling effector). betaarrestin then targets the receptors to the clathrin endocytosis pathway, and serves as an adaptor linking receptors to other signalling pathways. Internalization of receptors serves not only to remove desensitized receptors from the plasma membrane, but also to engage receptors in the resensitization pathway.
The internalization of Angiotensin II (Ang II) type 1 receptor (AT1R) is controversial and poorly described. Therefore, our laboratory studies the mechanisms behind AT1R internalization. The agonist-induced internalization of AT1R begins with the formation of a complex including betaarrestin, the clathrin adaptor AP-2, and the tyrosine protein kinase, c-Src. In turn, this c-Src recruitment regulates the clathrin-mediated internalization of AT1R by controlling the formation of endocytic complexes during endocytosis. Indeed, the recruitment of c-Src is involved in the dissociation of AP-2 during receptor internalization. Based on our evidence that AP-2 and c-Src can be found in the same complex, we suggested that AP-2 could be phosphorylated by c-Src. Indeed, we found that Ang II induced the c-Src-mediated tyrosine phosphorylation of the beta-subunit of AP-2 (beta2-adaptin). We were able to map one of the tyrosines in beta2-adaptin and assess its role in regulating the binding of its principal partner: betaarrestin. The phosphorylation state of beta2-adaptin dictates its association profile with betaarrestin: when phosphorylated it reduces its binding to betaarrestin. Finally, we proposed a model for AT1R internalization. Overall, these studies are significant because they allow a better understanding of the underlying mechanism that regulates the initial steps of clathrin-coated vesicle endocytosis of AT1R.
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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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RAZAGHI, AHMAD. "Les proteines apparentees a l'antigene-s/arrestine : une nouvelle famille de proteines." Paris 6, 1992. http://www.theses.fr/1992PA066592.

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L'antigene-s (arrestine ou proteine 48 k) a ete considere comme un constituant specifique des photorecepteurs de la retine et des cellules de l'organe pineal, qui derivent phylogenetiquement de photorecepteurs. Dans les batonnets retiniens, il participe a la regulation de la phototransduction en se liant a la rhodopsine photoactivee et phosphorylee. L'antigene-s apparait aujourd'hui comme l'un des membres d'une famille de proteines qui auraient des fonctions regulatrices semblables dans differents systemes de transduction. 1) nous purifions a partir de glande pineale de buf une proteine dont les proprietes, y compris le pouvoir d'induire l'uveo-retinite auto-immune experimentale, semblent identiques a celles de l'antigene-s de retine. 2) nous caracterisons et purifions des proteines immunoreactives avec des anticorps diriges contre l'antigene-s de retine dans differentes cellules et tissus: erythrocytes d'oiseau et de poisson, myocarde de buf, rein de buf et de rat, plaquettes sanguines humaines, cellules de tabac et chlamydomonas. 3) nous montrons que ces proteines apparentees de differentes origines partagent la propriete de se lier a la rhodopsine phosphorylee. Il semble que des membres de cette famille de proteines soient presents dans l'ensemble du monde vivant. Leur connaissance progressera avec l'isolement de leurs genes et l'etude de leurs fonctions, qui sont actuellement entrepris
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Lake, David Jonathan. "A human alpha-arrestin protein with a potential role in cargo protein trafficking within the endocytic system." Thesis, University of Nottingham, 2013. http://eprints.nottingham.ac.uk/13335/.

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β-Arrestins are essential adaptors for G protein-coupled receptor (GPCR) trafficking. Evolutionary ancestors of the β-arrestins – dubbed α-arrestins – are present in yeast/fungi and, similar to β-arrestins, recognise cargo proteins and mediate their intracellular trafficking. Mammalian α-arrestins include five largely uncharacterised arrestin domain-containing (ARRDC1-5) proteins that display a predicted arrestin structure; the current study focuses on human ARRDC2. Confocal microscopy of exogenous, fluorescent protein-tagged ARRDC2 in U2OS cells in combination with compartment-specific markers indicated that ARRDC2 is dynamically distributed throughout the plasma membrane and endocytic system, predominantly to late endosomes/lysosomes. Anti-ARRDC2 immunostaining in several primary cell lines broadly supported this conclusion. ARRDC2 contains two proline-rich (PPxY) motifs that in other α-arrestins have been reported to mediate interactions with WW domain-containing NEDD4 family E3 ubiquitin ligases. Coimmunoprecipitation indicated that ARRDC2 is able to interact with several NEDD4 E3s via its PPxY motifs, and confocal microscopy suggested that this interaction may influence the subcellular targeting of the ligases. Ubiquitination of ARRDC2 was detected by coimmunoprecipitation, although this modification was independent of ARRDC2 interaction with NEDD4 E3s. ARRDC2 colocalised with agonist-stimulated, internalised GPCRs (β2-adrenergic receptor (β2AR) and δ-opioid receptor (δOR)) and colocalisation analysis indicated that this involved compartmental redistribution of ARRDC2 to receptor-containing early/recycling endosomes, suggesting a specific effect. Interaction of ARRDC2 with δOR was detected using coimmunoprecipitation, and confocal analysis suggested that ARRDC2 may influence δOR and β2AR intracellular trafficking. ARRDC2 was also found to oligomerise with itself and the β-arrestins. Confocal microscopy showed that ARRDC2 overexpression can induce the redistribution of β-arrestin1 to ARRDC2-positive vesicles, and a punctate bimolecular fluorescence complementation (BiFC) signal was detected between ARRDC2 and β-arrestin2. From this, it is speculated that α-/β-arrestins may function cooperatively or competitively to mediate discrete GPCR sorting events in the endocytic pathway.
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Witty, Marie-France. "Role of the adaptor protein, beta-arrestin1, in the Notch signaling pathway." Thesis, University of British Columbia, 2007. http://hdl.handle.net/2429/446.

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The Notch receptor is part of a highly conserved signaling pathway shared in Drosophila, C. elegans and mammals. Extensive studies of Notch signaling have revealed its participation in the development of diverse organ systems including brain, blood cells, blood vessels, gut, and skin. Many genetic modifiers of the Notch signaling pathway have been identified, including some which act at the membrane and others in the nucleus. One such member is Deltex, an E3 ubiquitin ligase, which was originally identified as a modifier of Notch in a Drosophila genetic screen. In early lymphoid development, Deltex has been demonstrated functionally to antagonize Notch signaling but the precise molecular mechanism for this functional antagonism between Notch and Deltex is not understood. However, in Drosophila, recent data supports the formation of a trimeric complex between Deltex, Kurtz and Notch that promotes Notch ubiquitin-mediated proteosomal degradation. Beta-arrestin1 is one of the closest mammalian homologues of Kurtz and functions as an adaptor protein in a variety of cellular processes such as endocytosis, ubiquitination and nuclear shuttling. We hypothesize that a similar interaction occurs in mammalian cells between Notch, beta-arrestin1 and Deltex to negatively modulate the Notch signaling pathway. Our data reveal a physical interaction between beta-arrestin1 and the Notch receptor. We could not, however, detect an interaction between Deltex and beta-arrestin1 by co-immunoprecipitation. We also demonstrate that Notch and beta-arrestin1 physically associate with both a membrane-bound form of activated Notch, as well as the intracellular form of Notch after membrane cleavage. Using RNA interference, as well as overexpression of beta-arrestin1, we demonstrate that beta-arrestin1 negatively regulates a Notch/CSL dependant reporter assay. We also show that the presence of Deltex enhances the negative modulation of the Notch signaling pathway mediated by beta-arrestin1. Therefore, we reveal a new Notch interacting protein and a novel role for beta-arrestin1 in the Notch signaling pathway.
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Books on the topic "Arrestin Proteins"

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(Organization), Human Rights Watch. "We are afraid to even look for them": Enforced disappearances in the wake of Xinjiang's protests. New York: Human Rights Watch, 2009.

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Beta-Arrestins: Methods and Protocols. Humana, 2019.

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Luttrell, Louis M. Molecular Biology of Arrestins. Elsevier Science & Technology Books, 2013.

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Luttrell, Louis M. Molecular Biology of Arrestins. Elsevier Science & Technology Books, 2013.

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Hattori, Yuichi, and Martin C. Michel, eds. G Protein-Coupled Receptor Kinases (GRKs) and Beta-Arrestins: New Insights into Disease Regulators. Frontiers Media SA, 2020. http://dx.doi.org/10.3389/978-2-88963-547-4.

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Lock Me Up or Let Me Go: The Protests, Arrest and Trial of an Environmental Activist. Raincoast Books, Press Gang Publishers, 2002.

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Cohn, Jr., Samuel K. Plague since 1894. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198819660.003.0015.

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The plague riots in India, which amassed crowds of up to 10,000, followed by strikes and shop closures, were larger than cholera’s, and arrests and executions could also surpass cholera-related repression. Occasionally, myths spread of doctors poisoning Indians or selling their body parts for cures, and some have concluded that plague and cholera riots were much the same. They were not. While cholera violence drove deep wedges into the fabric of societies, plague riots united communities, even Muslims and Hindus, in common cause against abusive military searches and colonial measures that violated religious customs, destroyed property, and humiliated women. In contrast to cholera riots, which showed few signs of pre-planning or leadership, petitions, peaceful demonstrations, and efforts to negotiate usually preceded the plague protests. Unlike cholera riots, plague protests did not turn on distrust of Western medicine. Instead, Indians lambasted governments for not pursuing the latest scientific findings.
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Baracos, Vickie E., Sharon M. Watanabe, and Kenneth C. H. Fearon. Aetiology, classification, assessment, and treatment of the anorexia-cachexia syndrome. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199656097.003.0205.

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Anorexia-cachexia is a heterogeneous and multifactorial syndrome most likely driven by systemic inflammation and neuroendocrine activation. Key diagnostic features include reduced appetite, weight loss, and muscle wasting. Key clinical problems include management of anorexia without resort to artificial nutritional support, and muscle wasting that cannot be completely arrested/reversed even with such intervention. Assessment should cover domains such as body stores of energy and protein, food intake, performance status, and factors resulting in excess catabolism. Intervention should be early rather than late, informed by the assessment process and focused on a multimodal approach (nutrition, exercise, and pharmacological agents). This chapter aims to discuss these issues and provide (a) the reader with some background principles to classification, (b) a simple approach to patient assessment and a robust algorithm for basic multimodal treatment, and (c) an overview of the evidence base for different pharmacological interventions.
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Sharfstein, Joshua M. HIV. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780190697211.003.0005.

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The emergence of AIDS in the early 1980s caused a profound crisis for federal health agencies, particularly the National Institutes of Health (NIH) and the U.S. Food and Drug Administration (FDA). Activists in ACT UP, charging that these agencies were failing patients with AIDS, initiated a series of escalating protests. NIH officials, led by Dr. Anthony Fauci, began to talk with the advocates and make major changes in the research process. However, over at the FDA, a protest involving the arrest of hundreds of AIDS activists undermined the agency’s public health image. Eventually, under a new commissioner, the FDA earned back the trust of activists.
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Groves, Danja S., and Charles G. Durbin. The surgical airway in the ICU. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0082.

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Tracheostomy is the most commonly performed (elective) surgical procedure in critically-ill patients. Compared with translaryngeal intubation, tracheostomy improves patient comfort, and leads to shorter length of intensive care unit and hospital stay. It relieves upper airway obstruction, protects the larynx and upper airway from damage, allows access to the lower airway for secretion removal, and provides a stable airway for patients requiring prolonged mechanical ventilation or oxygenation support. Timing of tracheostomy remains controversial and should be individualized; however, early tracheostomy (within 7 days) seems to be beneficial in certain patient populations (head injury, medically critically ill). The evolution of percutaneous techniques are rapidly reducing need for surgical tracheostomy and bedside techniques are safe and efficient, allowing timely tracheostomy with low morbidity. Cricothyrotomy is an emergency surgical airway used to save a life when all attempts at securing a patent airway fail and arrest is eminent. Techniques, timing, risks, benefits, as well as contraindications of the surgical airway in critically-ill patients are discussed in this chapter.
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Book chapters on the topic "Arrestin Proteins"

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Perry, Nicole A., Xuanzhi Zhan, T. M. Iverson, Eugenia V. Gurevich, and Vsevolod V. Gurevich. "Monofunctional Elements of Multi-functional Proteins." In The Structural Basis of Arrestin Functions, 255–71. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-57553-7_18.

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Nato, A., A. Mirshahi, J. M. Cavalcante Alves, D. Lavergne, G. Ducreux, M. Mirshahi, J. P. Faure, et al. "Are Arrestin-Like Proteins Involved in Plant Signal Transduction Pathways?" In Current Issues in Plant Molecular and Cellular Biology, 519–24. Dordrecht: Springer Netherlands, 1995. http://dx.doi.org/10.1007/978-94-011-0307-7_71.

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Lefkowitz, R. J., and M. G. Caron. "The Role of Receptor Kinases and Arrestin-Like Proteins in G-Protein-Linked Receptor Desensitization." In GTPases in Biology II, 33–42. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-78345-6_3.

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Alexander, Revu Ann, Isaure Lot, and Hervé Enslen. "Methods to Characterize Protein Interactions with β-Arrestin In Cellulo." In Beta-Arrestins, 139–58. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9158-7_9.

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Bourquard, Thomas, Astrid Musnier, Aurélie Tréfier, Flavie Landomiel, Thomas Boulo, Eric Reiter, Pascale Crépieux, and Anne Poupon. "Methods to Determine Interaction Interfaces Between β-Arrestins and Their Protein Partners." In Beta-Arrestins, 177–94. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9158-7_12.

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Nagi, Karim, and Sudha K. Shenoy. "Detection of β-Arrestin-Mediated G Protein-Coupled Receptor Ubiquitination Using BRET." In Beta-Arrestins, 93–104. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9158-7_6.

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Fillion, Dany, Dominic Devost, and Terence E. Hébert. "Measuring Recruitment of β-Arrestin to G Protein-Coupled Heterodimers Using Bioluminescence Resonance Energy Transfer." In Beta-Arrestins, 83–91. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9158-7_5.

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Perry, Nicole A., Xuanzhi Zhan, Eugenia V. Gurevich, T. M. Iverson, and Vsevolod V. Gurevich. "Using In Vitro Pull-Down and In-Cell Overexpression Assays to Study Protein Interactions with Arrestin." In Beta-Arrestins, 107–20. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9158-7_7.

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Cao, Yubo, Yoon Namkung, and Stéphane A. Laporte. "Methods to Monitor the Trafficking of β-Arrestin/G Protein-Coupled Receptor Complexes Using Enhanced Bystander BRET." In Beta-Arrestins, 59–68. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9158-7_3.

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Gurevich, Eugenia V., and Vsevolod V. Gurevich. "Therapeutic Potential of Small Molecules and Engineered Proteins." In Arrestins - Pharmacology and Therapeutic Potential, 1–12. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-41199-1_1.

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Conference papers on the topic "Arrestin Proteins"

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Hua, Kuo-Tai, Michael Hsiao, and Min-Liang Kuo. "Abstract 3376: Human arrest defective 1 protein suppresses cancer cell metastasis by binding PIX/Cool proteins and inhibiting Cdc42/Rac1 activity." 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.am10-3376.

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Bieniek, Jared, Chandra Childress, Matthew Swatski, and Wannian Yang. "Abstract 4546: COX-2 inhibitors arrest prostate cancer cell cycle progression by downregulation of kinetochore/centromere proteins." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-4546.

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Nickkholgh, Bita, Sivanandane Sittadjody, Michael B. Rothberg, and KC Balaji. "Abstract LB-243: Protein kinase D1 induces cell cycle arrest independent from check point kinases." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-lb-243.

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Owens, Philip, Agniesszka E. Gorska, Mary E. Aakre, and Harold L. Moses. "Abstract 3840: Bone morphogenetic proteins require the type II TGFβ receptor for growth arrest in mammary tumor cells." 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.am10-3840.

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Korner, G., and Thorir D. Bjornsson. "INTRACELLULAR REGULATION OF TRANSGLUTAMINASE IN INTACT AND H202 INJURED CLONED BOVINE ENDOTHELIAL CELLS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642863.

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Vascular endothelial cells are normally in a quiescent, nonproliferating state. After intimal injury, they are likely to undergo proliferation. We found that cloned bovine aortic endothelial cells (EC) in culture contain high activity of tissue-type transglutaminase (TG). The enzyme was Ca++ dependent, the Km and vmax for putrescine were 0.203 and 18.5 nmol/min/mg protein. Primary amines were capable of inhibiting its activity but not methylated dansylcadaverine. EC and TG molecular weight estimated by gel filtration or by SDS-PAGE, was 88±5,000 Kd. Immunologically it was cross-reactive with purified rat liver TG. TG activity and antigen were found to increase significantly, when the cultures reached confluence and even more when cultures arrested at G0/G1 state by serum depletion. The half-life of EC-TG in G0/G1 arrested cultures was 128 minutes, determined in the presence cycloheximide; no decrease was observed in confluent cultures, indicating active accumulation of TG at the non-pro-liferative state. Most of cellular TG activity was found in the 15,000 g soluble fraction, with the crude membrane fraction containing 4-22% of the total TG activity, depending on the state of cell proliferation. However, immunoblots revealed that the membrane fraction contained similar amounts of TG antigen as did the soluble fraction. When the membranes were treated with detergents (0.1% SDS, 0.5 M NaCl, 75 mM KSCN, 75 mM dithio-threitol), the activity increased significantly, resulting in as much as 4- to 7-fold increases above control. Similar treatment of the soluble fraction did not increase TG activity. This data strongly suggests that the cell membranes contain a latent or cryptic form of TG that can undergo activation. Indeed, when cultures were injured by exposing them to H2O2 (10-10 mM) , a rapid 75-200% increase in TG activity was observed. One hour later, the activity was at control level. If protein synthesis inhibitors were present, no decrease was noted up to 8 hours. It is proposed that significant amounts of TG is stored in an inactive form in endothelial cell membranes, and that under different conditions, e.g., cell injury, activation and translocation of the enzyme can occur, out of and back into the cells membrane.
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Yuan, Ruixue. "Abstract A105: Checkpoint kinase 1 and 14-3-3 proteins inhibit atypical E2Fs to prevent a permanent cell cycle arrest." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; October 26-30, 2017; Philadelphia, PA. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1535-7163.targ-17-a105.

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Zambalde, Erika Pereira, Ana Carolina Rodrigues, Rubens Silveira Lima, Enilze Maria Souza Fonseca Ribeiro, and Jaqueline Carvalho Oliveira. "TLNC-UC.147, A NOVEL LONG RNA (lncRNA) FROM AN ULTRACONSERVED REGION AS POTENTIAL BIOMARKER IN LUMINAL A BREAST CANCER." In Scientifc papers of XXIII Brazilian Breast Congress - 2021. Mastology, 2021. http://dx.doi.org/10.29289/259453942021v31s1052.

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Introduction: Long RNAs are non-coding RNAs with more than 200 nucleotides in length, with essential regulatory roles in several biological processes, including in breast cancer (BC). The human genome contains 481 ultraconserved regions, which are genomic stretches of over 200 base pairs conserved among humans, rats, and mice. Most of these regions are transcriptionally active (T-UCRs), and several are differentially expressed in tumors. Some T-UCRs have been functionally characterized, but few have been associated with BC. Objectives: In this study, we aimed to expand the knowledge of T-UCRs in BC and characterize the lnc-uc.147, a long RNA transcribed from an ultraconserved region. Methods: We evaluated the expression level of 481 T-UCRs and their association with clinical parameters from TCGA data. For confirmation, 102 Brazilian BC samples were analyzed by RT-qPCR. Cytosolic and nuclear cell fractions and RT-qPCRs were done to determine the cell compartment of the transcript. Northern blotting and RACE were performed to determine the sequence and precise size of lnc-uc.147. Using two luminal cell lines (CAMA and BT474), a siRNA-based approach was applied to investigate the effects of lnc-uc.147 knockdown in cell viability, colony formation, and apoptosis level. To understand the interactions of lnc-uc.147 and proteins, we performed a pull-down assay. Results: Using TCGA (The Cancer Genome Atlas) data, we found 302 T-UCRs related to clinical features in BC: 43% were associated with molecular subtypes, 36% with estrogen-receptor positivity, 17% with HER2 expression, 12% with stage, and 10% with overall survival. We found that uc.147 is highly expressed in luminal A and B patients, which was also confirmed in Brazilian samples. For luminal A, a subtype usually associated with better prognosis, high uc.147 expression was associated with a poor prognosis and suggested as an independent prognostic factor. The lncRNA from uc.147 (lnc-uc.147) is in the nucleus. Northern blotting results show that uc.147 is a 2,8 kb monoexonic transcript. The silencing of uc.147 increases apoptosis, arrests the cell cycle and reduces cell viability and colony formation in luminal BC cell lines. Additionally, we identified 19 proteins that interact with uc.147 through mass spectrometry. These proteins are mainly involved in cytoskeletal and centrosome organization as well as in epithelial-mesenchymal transition. Conclusions: We show herein evidence that neoplastic BC cells exhibit a unique expression profile of T-UCRs. This study characterized the lnc-uc.147, a transcript that has never been described before. Indeed, lnc-uc.147 has an oncogenic effect in the luminal BC cell line and can interact with proteins. Furthermore, uc.147 has the potential as a BC prognostic marker in luminal patients.
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Gao, Li, and Jennie L. Williams. "Abstract 3817: Nitric oxide-donating aspirin induces G2/M phase cell cycle arrest in human cancer cells by regulating phase transition proteins." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-3817.

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Saba, Nakhle S., Roy S. Weiner, Hana F. Safah, and Laura S. Levy. "Abstract LB-308: Protein kinase C beta selective inhibition induces apoptosis and arrests cell cycle in acute lymphoblastic leukemia cell lines." 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-lb-308.

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Shrivastav, Meena, Jamie Ostrem, Mark M. Schroeder, Brett L. Carlson, and Jann N. Sarkaria. "Abstract 2898: Inhibition of heat shock protein 90 through HSP990 causes cell cycle arrest, growth inhibition, and apoptosis in glioblastoma tumors." 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.am2011-2898.

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Reports on the topic "Arrestin Proteins"

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Iwamoto, Yoshiki. Cell Growth Arrest Mediated by STAT Proteins in Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, July 1998. http://dx.doi.org/10.21236/ada358078.

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Rajabi, Hasan N. The Mechanism of Retinoblastoma Protein-Mediated Terminal Cell Cycle Arrest. Fort Belvoir, VA: Defense Technical Information Center, September 2003. http://dx.doi.org/10.21236/ada421731.

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Weiser, Douglas C. The Role of GADD34 (Growth Arrest and DNA Damage-Inducible Protein) in Regulating Apoptosis, Proliferation, and Protein Synthesis in Human Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, July 2004. http://dx.doi.org/10.21236/ada427916.

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Weiser, Douglas C. The Role of GADD34 (Growth Arrest and DNA Damage-Inducible Protein) in Regulating Apoptosis, Proliferation, and Protein Synthesis in Human Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, July 2003. http://dx.doi.org/10.21236/ada418759.

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Wang, Yuxun. Function of Human Selenium-Binding Protein in Selenium Induced Growth Arrest and Apoptosis in Prostate Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, April 2004. http://dx.doi.org/10.21236/ada437732.

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Debeljak, Natasa. Function of Human Selenium-Binding Protein in Selenium Induced Growth Arrest and Apoptosis in Prostate Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, April 2005. http://dx.doi.org/10.21236/ada442188.

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Weiss, David, and Neil Olszewski. Manipulation of GA Levels and GA Signal Transduction in Anthers to Generate Male Sterility. United States Department of Agriculture, 2000. http://dx.doi.org/10.32747/2000.7580678.bard.

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The original objectives of the research were: i. To study the role of GA in anther development, ii. To manipulate GA and/or GA signal transduction levels in the anthers in order to generate male sterility. iii. To characterize the GA signal transduction repressor, SPY. Previous studies have suggested that gibberellins (GAs) are required for normal anther development. In this work, we studied the role of GA in the regulation of anther development in petunia. When plants were treated with the GA-biosynthesis inhibitor paclobutrazol, anther development was arrested. Microscopic analysis of these anthers revealed that paclobutrazol inhibits post-meiotic developmental processes. The treated anthers contained pollen grains but the connective tissue and tapetum cells were degenerated. The expression of the GA-induced gene, GIP, can be used in petunia as a molecular marker to: study GA responses. Analyses of GIP expression during anther development revealed that the gene is induced only after microsporogenesis. This observation further suggests a role for GA in the regulation of post-meiotic processes during petunia anther development. Spy acts as a negative regulator of gibberellin (GA) action in Arabidopsis. We cloned the petunia Spy homologue, PhSPY, and showed that it can complement the spy-3 mutation in Arabidopsis. Overexpression of Spy in transgenic petunia plants affected various GA-regulated processes, including seed germination, shoot elongation, flower initiation, flower development and the expression of a GA- induced gene, GIP. In addition, anther development was inhibited in the transgenic plants following microsporogenesis. The N-terminus of Spy contains tetratricopeptide repeats (TPR). TPR motifs participate in protein-protein interactions, suggesting that Spy is part of a multiprotein complex. To test this hypothesis, we over-expressed the SPY's TPR region without the catalytic domain in transgenic petunia and generated a dominant- negative Spy mutant. The transgenic seeds were able to germinate on paclobutrazol, suggesting an enhanced GA signal. Overexpression of PhSPY in wild type Arabidopsis did not affect plant stature, morphology or flowering time. Consistent with Spy being an O-GlcNAc transferase (OGT), Spy expressed in insect cells was shown to O-GlcNAc modify itself. Consistent with O-GlcNAc modification playing a role in GA signaling, spy mutants had a reduction in the GlcNAc modification of several proteins. After treatment of the GA deficient, gal mutant, with GA3 the GlcNAc modification of proteins of the same size as those affected in spy mutants exhibited a reduction in GlcNAcylation. GA-induced GlcNAcase may be responsible for this de-GlcNAcylation because, treatment of gal with GA rapidly induced an increase in GlcNAcase activity. Several Arabidopsis proteins that interact with the TPR domain of Spy were identified using yeast two-hybrids screens. One of these proteins was GIGANTEA (GI). Consistent with GI and Spy functioning as a complex in the plant the spy-4 was epistatic to gi. These experiments also demonstrated that, in addition to its role in GA signaling, Spy functions in the light signaling pathways controlling hypocotyl elongation and photoperiodic induction of flowering. A second Arabidopsis OGT, SECRET AGENT (SCA), was discovered. Like SPY, SCA O-GlcNAc modifies itself. Although sca mutants do not exhibit dramatic phenotypes, spy/sca double mutants exhibit male and female gamete and embryo lethality, indicating that Spy and SCA have overlapping functions. These results suggest that O-GlcNAc modification is an essential modification in plants that has a role in multiple signaling pathways.
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Hassumani, Daniel. Expression of Growth Arrest and DNA Damage Protein 45-alpha (gadd45-alpha) and the CCAAT/enhancer binding protein-delta (C/EBP-delta) in Fishes Exposed to Heat and Hypoxia. Portland State University Library, January 2000. http://dx.doi.org/10.15760/etd.943.

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Chejanovsky, Nor, and Suzanne M. Thiem. Isolation of Baculoviruses with Expanded Spectrum of Action against Lepidopteran Pests. United States Department of Agriculture, December 2002. http://dx.doi.org/10.32747/2002.7586457.bard.

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Our long-term goal is to learn to control (expand and restrict) the host range of baculoviruses. In this project our aim was to expand the host range of the prototype baculovirus Autographa cali/arnica nuclear polyhedrosis virus (AcMNPV) towards American and Israeli pests. To achieve this objective we studied AcMNPV infection in the non-permissive hosts L. dispar and s. littoralis (Ld652Y and SL2 cells, respectively) as a model system and the major barriers to viral replication. We isolated recombinant baculoviruses with expanded infectivity towards L. dispar and S. littoralis and tested their infectivity towards other Lepidopteran pests. The restricted host range displayed by baculoviruses constitutes an obstacle to their further implementation in the control of diverse Lepidopteran pests, increasing the development costs. Our work points out that cellular defenses are major role blocks to AcMNPV replication in non- and semi-permissive hosts. Therefore a major determinant ofbaculovirus host range is the ability of the virus to effectively counter cellular defenses of host cells. This is exemplified by our findings showing tliat expressing the viral gene Ldhrf-l overcomes global translation arrest in AcMNPV -infected Ld652Y cells. Our data suggests that Ld652Y cells have two anti-viral defense pathways, because they are subject to global translation arrest when infected with AcMNPV carrying a baculovirus apoptotic suppressor (e.g., wild type AcMNPV carryingp35, or recombinant AcMNPV carrying Opiap, Cpiap. or p49 genes) but apoptose when infected with AcMNPV-Iacking a functional apoptotic suppressor. We have yet to elucidate how hrf-l precludes the translation arrest mechanism(s) in AcMNPV-infected Ld652Y cells. Ribosomal profiles of AcMNPV infected Ld652Y cells suggested that translation initiation is a major control point, but we were unable to rule-out a contribution from a block in translation elongation. Phosphorylation of eIF-2a did not appear to playa role in AcMNPV -induced translation arrest. Mutagenesis studies ofhrf-l suggest that a highly acidic domain plays a role in precluding translation arrest. Our findings indicate that translation arrest may be linked to apoptosis either through common sensors of virus infection or as a consequence of late events in the virus life-cycle that occur only if apoptosis is suppressed. ~ AcMNPV replicates poorly in SL2 cells and induces apoptosis. Our studies in AcMNPV - infected SL2ceils led us to conclude that the steady-state levels of lEI (product of the iel gene, major AcMNPV -transactivator and multifunctional protein) relative to those of the immediate early viral protein lEO, playa critical role in regulating the viral infection. By increasing the IEl\IEO ratio we achieved AcMNPV replication in S. littoralis and we were able to isolate recombinant AcMNPV s that replicated efficiently in S. lifforalis cells and larvae. Our data that indicated that AcMNPV - infection may be regulated by an interaction between IE 1 and lED (of previously unknown function). Indeed, we showed that IE 1 associates with lED by using protein "pull down" and immunoprecipitation approaches High steady state levels of "functional" IE 1 resulted in increased expression of the apoptosis suppressor p35 facilitating AcMNPV -replication in SL2 cells. Finally, we determined that lED accelerates the viral infection in AcMNPV -permissive cells. Our results show that expressing viral genes that are able to overcome the insect-pest defense system enable to expand baculovirus host range. Scientifically, this project highlights the need to further study the anti-viral defenses of invertebrates not only to maximi~e the possibilities for manipulating baculovirus genomes, but to better understand the evolutionary underpinnings of the immune systems of vertebrates towards virus infection.
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Sadot, Einat, Christopher Staiger, and Mohamad Abu-Abied. Studies of Novel Cytoskeletal Regulatory Proteins that are Involved in Abiotic Stress Signaling. United States Department of Agriculture, September 2011. http://dx.doi.org/10.32747/2011.7592652.bard.

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Abstract:
In the original proposal we planned to focus on two proteins related to the actin cytoskeleton: TCH2, a touch-induced calmodulin-like protein which was found by us to interact with the IQ domain of myosin VIII, ATM1; and ERD10, a dehydrin which was found to associate with actin filaments. As reported previously, no other dehydrins were found to interact with actin filaments. In addition so far we were unsuccessful in confirming the interaction of TCH2 with myosin VIII using other methods. In addition, no other myosin light chain candidates were found in a yeast two hybrid survey. Nevertheless we have made a significant progress in our studies of the role of myosins in plant cells. Plant myosins have been implicated in various cellular activities, such as cytoplasmic streaming (1, 2), plasmodesmata function (3-5), organelle movement (6-10), cytokinesis (4, 11, 12), endocytosis (4, 5, 13-15) and targeted RNA transport (16). Plant myosins belong to two main groups of unconventional myosins: myosin XI and myosin VIII, both closely related to myosin V (17-19). The Arabidopsis myosin family contains 17 members: 13 myosin XI and four myosin VIII (19, 20). The data obtained from our research of myosins was published in two papers acknowledging BARD funding. To address whether specific myosins are involved with the motility of specific organelles, we cloned the cDNAs from neck to tail of all 17 Arabidopsis myosins. These were fused to GFP and used as dominant negative mutants that interact with their cargo but are unable to walk along actin filaments. Therefore arrested organelle movement in the presence of such a construct shows that a particular myosin is involved with the movement of that particular organelle. While no mutually exclusive connections between specific myosins and organelles were found, based on overexpression of dominant negative tail constructs, a group of six myosins (XIC, XIE, XIK, XI-I, MYA1 and MYA2) were found to be more important for the motility of Golgi bodies and mitochondria in Nicotiana benthamiana and Nicotiana tabacum (8). Further deep and thorough analysis of myosin XIK revealed a potential regulation by head and tail interaction (Avisar et al., 2011). A similar regulatory mechanism has been reported for animal myosin V and VIIa (21, 22). In was shown that myosin V in the inhibited state is in a folded conformation such that the tail domain interacts with the head domain, inhibiting its ATPase and actinbinding activities. Cargo binding, high Ca2+, and/or phosphorylation may reduce the interaction between the head and tail domains, thus restoring its activity (23). Our collaborative work focuses on the characterization of the head tail interaction of myosin XIK. For this purpose the Israeli group built yeast expression vectors encoding the myosin XIK head. In addition, GST fusions of the wild-type tail as well as a tail mutated in the amino acids that mediate head to tail interaction. These were sent to the US group who is working on the isolation of recombinant proteins and performing the in vitro assays. While stress signals involve changes in Ca2+ levels in plants cells, the cytoplasmic streaming is sensitive to Ca2+. Therefore plant myosin activity is possibly regulated by stress. This finding is directly related to the goal of the original proposal.
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