Relevant bibliographies by topics / ?-arrestin

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic '?-arrestin'

Author: Grafiati
Published: 4 June 2021
Last updated: 25 July 2025

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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 (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 t
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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 (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 p
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Rakib, Ahmed, Taslima Akter Eva, Saad Ahmed Sami, et al. "Beta-Arrestins in the Treatment of Heart Failure Related to Hypertension: A Comprehensive Review." Pharmaceutics 13, no. 6 (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-adre
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Li, Dongjun, and Donna Woulfe. "Arrestin-2 Differentially Regulates PAR4 and P2Y12 Receptor Signaling in Platelets." Blood 112, no. 11 (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 animal
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Bhattacharya, Somdatta, Joydeep Paul, Srijan Haldar та Kuntal Pal. "Residue-specific orientation of arrestin in 5-HTR1B (Serotonin Receptor)- βArrestin-1 interaction". Journal of Experimental Biology and Agricultural Sciences 12, № 1 (2024): 138–44. http://dx.doi.org/10.18006/2024.12(1).138.144.

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Physiologically G protein-coupled receptors (GPCRs) are an important class of cell surface proteins capable of sensing the exogenous signals across the cell membrane through G-protein-dependent and independent pathways. Activated GPCRs initiate diverse G-protein-independent signalling through interaction with arrestin. Arrestins comprise a family of four proteins that act as signal regulators of GPCRs. Arrestin specificity and assembly orientation with a particular GPCR depend on the finger loop's residues. Recent cryo-EM structural elucidation of neurotensin receptor-1(NTSR1)-β-arrestin1compl
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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 (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 re
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Cao, Yubo, Sahil Kumar, Yoon Namkung, Laurence Gagnon, Aaron Cho та Stéphane A. Laporte. "Angiotensin II type 1 receptor variants alter endosomal receptor–β-arrestin complex stability and MAPK activation". Journal of Biological Chemistry 295, № 38 (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 recep
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Zarca, Aurélien, Claudia Perez, Jelle van den Bor та ін. "Differential Involvement of ACKR3 C-Tail in β-Arrestin Recruitment, Trafficking and Internalization". Cells 10, № 3 (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: W
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Nakaya, Michio, Satsuki Chikura, Kenji Watari та ін. "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, № 42 (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
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Qu, Changxiu, Ji Young Park, Min Woo Yun, et al. "Scaffolding mechanism of arrestin-2 in the cRaf/MEK1/ERK signaling cascade." Proceedings of the National Academy of Sciences 118, no. 37 (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
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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
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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 thes
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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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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 ex
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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 Untersuchung
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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-
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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
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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 can
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Books on the topic "?-arrestin"

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

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Weyand, Ingo. Experimente zur Phosphorylierung und Mikroheterogenität von Arrestin (48-kDa Protein) aus Rinderretina. Zentralbibliothek der Kernforschungsanlage, 1988.

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

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Parker, Brenda. Arresting love. Thorpe, 1991.

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Luke, Allyn. Contaminant arresting systems. 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. Wolf Legal Productions, 2001.

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

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

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

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

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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. 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. 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. 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. 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. 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. 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, et al. "Self-Association of Arrestin Family Members." In Arrestins - Pharmacology and Therapeutic Potential. 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. 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. 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. 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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Davison, Nigel, Adrian Roberts, and Gareth Glass. "Arresting and Preventing Corrosion of Steel in Concrete*." In CORROSION 2008. NACE International, 2008. https://doi.org/10.5006/c2008-08302.

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Abstract Corrosion of steel reinforcement is a major factor affecting the durability of reinforced concrete structures. To address this problem an improved electrochemical treatment consisting of two phases has been developed. Firstly a high current is briefly driven to the steel to arrest corrosion. In the process corroding sites are moved from the steel to an installed anode system. This first phase lasts about 1 week. Galvanic protection is then provided. This is low maintenance and requires no user intervention to function. A single anode system consisting of a hybrid of impressed current
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Piatkowski, David M., J. Peter Ault, and John Travaglini. "Service Life Extension of E-28 Arresting Gear Systems." In CORROSION 2001. NACE International, 2001. https://doi.org/10.5006/c2001-01570.

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Abstract Naval Air Warfare Center wants to extend the service life of their E-28 Shore-Based Arresting Gear Systems. The present life expectancy of the system is approximately 10 to 15 years. The goal of this effort is to increase that life to 20+ years and to reduce maintenance and replacement costs. Central to the life extension program is increasing the corrosion resistance of the hydraulic absorbers that hold the hydraulic fluid used for resistance. To improve the corrosion durability of this equipment, a research program was developed to test candidate coating systems and cathodic protect
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Akhormeh, Alireza Naderi, Davide Geoffrey Svampa, Fabio Pera, et al. "Wearable Drone as a Fall Arresting Device: Preliminary Concept and Feasibility Analysis." In 2024 20th IEEE/ASME International Conference on Mechatronic and Embedded Systems and Applications (MESA). IEEE, 2024. http://dx.doi.org/10.1109/mesa61532.2024.10704865.

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Boudria, Yacine, Raymond Sepe, and Steven P. Bastien. "Trajectory and Binning Strategy with LQG/LTR Controller for Aircraft Arresting Gear System." In 2024 AIAA DATC/IEEE 43rd Digital Avionics Systems Conference (DASC). IEEE, 2024. http://dx.doi.org/10.1109/dasc62030.2024.10749395.

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Scannell, William T., Ali Akbar Sohanghpurwala, Rodney G. Powers, and William H. Hartt. "Cathodic Protection of Prestressed Concrete Bridge Pilings in a Marine Environment." In CORROSION 1994. NACE International, 1994. https://doi.org/10.5006/c1994-94305.

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Abstract Cathodic protection (CP) is the only recognized technique for arresting ongoing corrosion of conventional mild reinforcing steel in concrete. This paper discusses the present state of knowledge regarding the applicability of this technology to prestressing steel. Practical and technical issues to consider in selecting a CP system for prestressed concrete bridge pilings in a marine environment are discussed. The design parameters for the first full scale installation of CP on over 170 prestressed concrete bridge pilings in a marine environment are presented. Performance data obtained o
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Miller, Kyle W., Qiuyan Chen, and Shuaitong Zhao. "Structural Basis of Arrestin and Membrane Interaction." In ASPET 2023 Annual Meeting Abstracts. American Society for Pharmacology and Experimental Therapeutics, 2023. http://dx.doi.org/10.1124/jpet.122.568360.

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Pacheco, Jonathan, and Jean-Pierre Vilardaga. "PTH–GPCR–arrestin complexes assembly in selective cell membrane spots." In ASPET 2024 Annual Meeting Abstract. American Society for Pharmacology and Experimental Therapeutics, 2024. http://dx.doi.org/10.1124/jpet.570.811350.

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Nibley, Preston C., Poonam Kumari, Annie Bao, et al. "Molecular Determinants of Beta-Arrestin Binding to the Glucagon Receptor." In ASPET 2024 Annual Meeting Abstract. American Society for Pharmacology and Experimental Therapeutics, 2024. http://dx.doi.org/10.1124/jpet.169.130707.

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Akins-Rivers, E. Joy, Nikia Smith та 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". У 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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Reports on the topic "?-arrestin"

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Jones, Alan. VPS26 Moonlights as an Arrestin-like Adapter for a 7-transmembrane RGS 2 protein in Arabidopsis thaliana. Office of Scientific and Technical Information (OSTI), 2023. http://dx.doi.org/10.2172/1959926.

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Hamid, Shahirah, ed. Arresting the decline in police trust. Monash University, 2023. http://dx.doi.org/10.54377/f1d0-fbae.

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Civale, L., L. Krusin-Elbaum, A. D. Marwick, et al. Arresting vortex motion in YBaCuO crystals with splay in columnar defects. Office of Scientific and Technical Information (OSTI), 1994. http://dx.doi.org/10.2172/204571.

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4

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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5

Wagener, Brant M. The Role of CXCR4 and Arrestins in Breast Cancer Signaling and Apoptosis. Defense Technical Information Center, 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. Defense Technical Information Center, 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. National Bureau of Economic Research, 2010. http://dx.doi.org/10.3386/w16460.

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8

Floyd, Webster, and Andrew Ward. Mobile Runway Edge Sheave Anchor criteria in asphalt concrete pavement. Engineer Research and Development Center (U.S.), 2025. https://doi.org/10.21079/11681/49724.

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Abstract:
The Mobile Runway Edge Sheave (MRES) is used in conjunction with the Mobile Aircraft Arresting System (MAAS) for setback aircraft arresting system (AAS) installations in expedient or temporary situations. There are existing criteria and tactics, techniques, and procedures (TTPs) for MRES installations on portland cement concrete (PCC) pavement and soil, but these criteria have not been developed for asphalt concrete (AC) pavements. The US Air Force Civil Engineer Center (AFCEC) tasked the US Army Engineer Research and Development Center (ERDC) to develop anchor criteria for the MRES in AC pave
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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.), 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. Defense Technical Information Center, 2009. http://dx.doi.org/10.21236/ada508608.

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