Literatura académica sobre el tema "?-arrestin"
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Artículos de revistas sobre el tema "?-arrestin"
Santini, F., R. B. Penn, A. W. Gagnon, J. L. Benovic y J. H. Keen. "Selective recruitment of arrestin-3 to clathrin coated pits upon stimulation of G protein-coupled receptors". Journal of Cell Science 113, n.º 13 (1 de julio de 2000): 2463–70. http://dx.doi.org/10.1242/jcs.113.13.2463.
Texto completoJAHNS, Roland, Franck BORGESE, Sabine LINDENTHAL, Annette STRAUB, René MOTAIS y 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, n.º 2 (1 de junio de 1996): 497–506. http://dx.doi.org/10.1042/bj3160497.
Texto completoRakib, Ahmed, Taslima Akter Eva, Saad Ahmed Sami, Saikat Mitra, Iqbal Hossain Nafiz, Ayan Das, Abu Montakim Tareq et al. "Beta-Arrestins in the Treatment of Heart Failure Related to Hypertension: A Comprehensive Review". Pharmaceutics 13, n.º 6 (5 de junio de 2021): 838. http://dx.doi.org/10.3390/pharmaceutics13060838.
Texto completoLi, Dongjun y Donna Woulfe. "Arrestin-2 Differentially Regulates PAR4 and P2Y12 Receptor Signaling in Platelets". Blood 112, n.º 11 (16 de noviembre de 2008): 110. http://dx.doi.org/10.1182/blood.v112.11.110.110.
Texto completoMorris, Gavin E., Carl P. Nelson, Paul J. Brighton, Nicholas B. Standen, R. A. John Challiss y 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, n.º 5 (1 de marzo de 2012): C723—C734. http://dx.doi.org/10.1152/ajpcell.00202.2011.
Texto completoCao, Yubo, Sahil Kumar, Yoon Namkung, Laurence Gagnon, Aaron Cho y Stéphane A. Laporte. "Angiotensin II type 1 receptor variants alter endosomal receptor–β-arrestin complex stability and MAPK activation". Journal of Biological Chemistry 295, n.º 38 (23 de julio de 2020): 13169–80. http://dx.doi.org/10.1074/jbc.ra120.014330.
Texto completoZarca, Aurélien, Claudia Perez, Jelle van den Bor, Jan Paul Bebelman, Joyce Heuninck, Rianna J. F. de Jonker, Thierry Durroux, Henry F. Vischer, Marco Siderius y Martine J. Smit. "Differential Involvement of ACKR3 C-Tail in β-Arrestin Recruitment, Trafficking and Internalization". Cells 10, n.º 3 (11 de marzo de 2021): 618. http://dx.doi.org/10.3390/cells10030618.
Texto completoNakaya, Michio, Satsuki Chikura, Kenji Watari, Natsumi Mizuno, Koji Mochinaga, Supachoke Mangmool, Satoru Koyanagi et al. "Induction of Cardiac Fibrosis by β-Blocker in G Protein-independent and G Protein-coupled Receptor Kinase 5/β-Arrestin2-dependent Signaling Pathways". Journal of Biological Chemistry 287, n.º 42 (10 de agosto de 2012): 35669–77. http://dx.doi.org/10.1074/jbc.m112.357871.
Texto completoQu, Changxiu, Ji Young Park, Min Woo Yun, Qing-tao He, Fan Yang, Kiae Kim, Donghee Ham et al. "Scaffolding mechanism of arrestin-2 in the cRaf/MEK1/ERK signaling cascade". Proceedings of the National Academy of Sciences 118, n.º 37 (10 de septiembre de 2021): e2026491118. http://dx.doi.org/10.1073/pnas.2026491118.
Texto completoKumar, P., C. S. Lau, M. Mathur, P. Wang y K. A. DeFea. "Differential effects of β-arrestins on the internalization, desensitization and ERK1/2 activation downstream of protease activated receptor-2". American Journal of Physiology-Cell Physiology 293, n.º 1 (julio de 2007): C346—C357. http://dx.doi.org/10.1152/ajpcell.00010.2007.
Texto completoTesis sobre el tema "?-arrestin"
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.
Texto completoAbstract : In an organism, intracellular [Ca2+] takes part in many biological processes. Eukaryotic cells express a variety of channels in the plasma membrane through which calcium can enter. In non-excitable cells, two main mechanisms allow calcium entry; the store-operated calcium entry via Orai1 (SOCE) and receptor-operated calcium entry (ROCE). Several key proteins are involved in the regulation of these calcium entry pathways as well as in calcium homeostasis. TRPC6 is a calcium channel implied in calcium entrance into the cells following hormonal stimulation and translocates to the plasma membrane. TRPC6 channel appear to the plasma membrane until the stimulus is present. Although, the mechanisms that regulate the trafficking and activation of TRPC6 are still little known. Recent findings have demonstrated that there is a potential role of Rho kinase in activity of TRPC6. Rho kinase is activated by the small G protein RhoA that itself can be activated by the heterotrimeric G proteins Gα12 and Gα13. In addition to Gα12 and Gα13 proteins, cytosolic GPCR desensitizing proteins β-arrestin 1 and/or β-arrestin 2 could also activate RhoA. The purpose of our study is to investigate the involvement of the proteins Gα12/13 and β-arrestin 1/β-arrestin 2 in the activation of TRPC6 and Orai1 protein. We used siRNA specific to Gα12/13 or β-arrestin 1/β-arrestin 2 to knockdown their endogenous expression. Then, calcium imaging in real time was performed in order to see the quantity of calcium entered into the cell following stimulation by vasopressin (AVP), thapsigargin, or carbachol. We hence identified that in A7r5 cell, vascular smooth muscle cell where TRPC6 channel expressed endogenously; reduced expression of Gα12 or Gα13 proteins does not seem to modify the AVP-induced Ca2+ entry compared to control cells. On the other hand, calcium imaging experiment in knocked down β-arrestin 1 or β-arrestin 2 in HEK 293 cells as well as HEK 293 cells stably transfected with TRPC6 (T6.11 cells) resulted in an increased thapsigargin-induced calcium entry. The co-immunoprecipitation studies demonstrate an interaction between β-arrestin 1 and STIM1, a calcium sensor in SOCE influx, while no interaction was observed between β-arrestin 1 and Orai1.We moreover showed by confocal microscopy that reduced expression of β-arrestin 1/ β-arrestin 2 does not influence the quantity of Orai1 at the cell periphery. Preliminary results showed that reduced expression of β-arrestin 1 or β-arrestin 2 increases the quantity of STIM1-YFP in the intracellular space and less it’s in peri-membrane space. In conclusion, we showed that β-arrestin 1 or β-arrestin 2 are involved in the store-operated calcium entry (SOCE) and control the quantity of STIM1 in the endoplasmic reticulum.
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.
Texto completoCarter, 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.
Texto completoEidhoff, 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.
Texto completoCorrell, Jennifer A. "Nicotine Sensitization in β-Arrestin 2 Knockout Adolescent Mice". Digital Commons @ East Tennessee State University, 2007. https://dc.etsu.edu/etd/2050.
Texto completoLally, Ciara. "Structural and functional characterization of the arrestin-rhodopsin complex". Doctoral thesis, Humboldt-Universität zu Berlin, 2017. http://dx.doi.org/10.18452/18570.
Texto completoThe protein arrestin is responsible for termination of GPCR signalling. In the rod cell, arrestin binds light-activated phosphorylated rhodopsin in order to block further signal transduction. The binding of arrestin to rhodopsin is a two-step process. Arrestin first interacts with the phosphorylated receptor C-terminus in a pre-complex, which induces conformational changes in arrestin that allow coupling to the helical core of the active receptor in a high-affinity complex. Biochemical studies and crystal structures have provided insights into the conformation of the arrestin-rhodopsin complex. This dissertation describes site-directed fluorescence experiments, which were carried out to further investigate the conformational changes occurring upon arrestin binding to rhodopsin and the nature of different binding modes of the arrestin-rhodopsin interaction. In particular this involved characterization of a previously unidentified association of arrestin with the membrane, as well as further elucidation of the structure of the pre-complex. The conformation of arrestin in the pre-complex is indicated to resemble that of the basal state of arrestin, and involves two sites of contact: interaction with the phosphorylated receptor C-terminus, and association with the membrane. Upon transition to the high-affinity complex, arrestin undergoes a conformational change to a more active conformation: the auto-inhibitory C-tail is displaced, there is movement within the central flexible loops, and the orientation of the membrane anchor changes. The pre-complex therefore most likely functions to bring arrestin and the receptor into close contact, and in the correct orientation, to allow for fast transition to the high-affinity complex.
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.
Texto completoThe loss of function and mass of pancreatic beta-cells play a central role in type 2 diabetes (T2D). Beta-arrestin 1 and 2 (ARRB1 and ARRB2) are involved in insulin secretion and/or beta-cell survival. In a first study, in order to characterize the role of ARRB1 in beta-cells, we aimed to invalidate the Arrb1 gene specifically in these cells using the Cre/lox system under the control of the Ins1 promoter. Studies had been published with both Ins1Cre-/+ and Arrb1f/f lines. We generated Arrb1f/f:Ins1Cre-/+ mice. The phenotype of Arrb1f/f :Ins1Cre-/+ mice was weak with a lack of reproducibility compared to Arrb1f/f :Ins1Cre-/- mice used as controls. The low expression level of Arrb1 in beta-cells and the lack of specific antibody for immunocytochemistry made it difficult to verify the absence of expression of ARRB1 in these cells. After sequencing the modified Arrb1 gene of the “floxed” mice, we observed that the insertion of the first loxP site induced a shift in the reading frame introducing a stop codon and, consequently, the non-expression of the Arrb1 gene. Since the “floxed“ Arrb1 mice used as controls were already knockout (KO), the project using these mice was stopped.Our team has reported the involvement of ARRB2 in the regulation of beta-cell mass, but its role in Glucagon-Like Peptide-1 (GLP-1) receptor signaling, a major therapeutic target for T2D, remained to be explored. In a second study, we showed a better glucose tolerance and an increase in insulin secretion from isolated islets in Arrb2KO compared to control mice in the presence of physiological circulating concentrations of GLP-1. This was correlated with higher cAMP production and PKA activation in Arrb2KO beta-cells. By contrast, the activation of ERK1/2 kinases was decreased indicating a major recruitment of ERK1/2 by ARRB2 to GLP-1R. In parallel, we showed that the expression levels of ARRB1 and ARRB2 in pancreatic islets were altered in diabetogenic and diabetic conditions. My results clearly demonstrate a critical role of ARRB2 in GLP-1R singaling which could impact the function, maintenance and plasticity of beta-cell mass in response to GLP-1. A lack of expression of ARRB2 could participate in the deficit of compensatory mechanisms of the functional beta-cell mass leading to T2D
Puca, Loredana. "Role of the arrestin family in notch pathway in mammals". Paris 6, 2013. http://www.theses.fr/2013PA066350.
Texto completoNotch signaling is an evolutionary conserved pathway implicated in embryonic development and in adult tissue homeostasis. A number of post-translational modifications have been implicated in regulating the activity of Notch receptor and some of them affect the degradation of non-activated Notch receptor. The starting points of my PhD project are Drosophila findings showing that the adaptor protein Kurtz, the unique non-visual arrestin in Drosophila, is an essential regulator of Notch signaling. In mammals the arrestin family (excluding the visual arrestins) is composed of two sub-families: -arrestins and-arrestins. The main results that I have obtained show that both -arrestins and -arrestins are recruited to non-activated Notch receptor and allow Itch-mediated Notch ubiquitination in mammals. Biochemical evidence shows that an heterodimerization between -arrestins and the -arrestin ARRDC1 is required to promote Notch ubiquitination and its lysosomal degradation. To conclude, we show for the first time that the --arrestin heterodimer is functionally involved in the degradation of Notch receptor, highlighting the existence of a cooperation between these adaptor proteins to regulate receptor trafficking
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.
Texto completoArmando, 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.
Texto completoG 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
Libros sobre el tema "?-arrestin"
Gurevich, Vsevolod V., ed. The Structural Basis of Arrestin Functions. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-57553-7.
Texto completoScott, Mark G. H. y Stéphane A. Laporte, eds. Beta-Arrestins. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9158-7.
Texto completoParker, Brenda. Arresting love. Anstey: Thorpe, 1991.
Buscar texto completoLuke, Allyn. Contaminant arresting systems. Trenton, NJ: New Jersey Dept. of Transportation, 2002.
Buscar texto completoDijk, W. A. M. van., Hovens J. L y Netherlands Koninklijke Marechaussee, eds. Arresting war criminals. Nijmegen: Wolf Legal Productions, 2001.
Buscar texto completoTraldi, Andrea. Gli arresti domiciliari. Roma: Ianua, 1988.
Buscar texto completoUpadhyay, Samrat. Arresting God in Kathmandu. New Delhi: Rupa & Co., 2002.
Buscar texto completoJoint Commission on Accreditation of Healthcare Organizations., ed. Tuberculosis: Arresting everyone's enemy. 2a ed. Oakbrook Terrace, IL: Joint Commission Resources, 2007.
Buscar texto completoArresting God in Kathmandu. Boston: Houghton Mifflin, 2001.
Buscar texto completoJoint Commission on Accreditation of Healthcare Organizations., ed. Tuberculosis: Arresting everyone's enemy. Oakbrook Terrace, IL: Joint Commission on Accreditation of Healthcare Organizations, 1996.
Buscar texto completoCapítulos de libros sobre el tema "?-arrestin"
Craft, Cheryl Mae y Janise D. Deming. "Cone Arrestin: Deciphering the Structure and Functions of Arrestin 4 in Vision". En Arrestins - Pharmacology and Therapeutic Potential, 117–31. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-41199-1_6.
Texto completoWillis, Miranda J. y George S. Baillie. "Arrestin-Dependent Localization of Phosphodiesterases". En Arrestins - Pharmacology and Therapeutic Potential, 293–307. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-41199-1_15.
Texto completoCameron, Ryan T. y George S. Baillie. "Arrestin Regulation of Small GTPases". En Arrestins - Pharmacology and Therapeutic Potential, 375–85. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-41199-1_19.
Texto completoKenakin, Terry. "Quantifying Biased β-Arrestin Signaling". En Arrestins - Pharmacology and Therapeutic Potential, 57–83. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-41199-1_3.
Texto completoZhao, Yang y Kunhong Xiao. "Proteomic Analysis of the β-Arrestin Interactomes". En Beta-Arrestins, 217–32. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9158-7_14.
Texto completoStrungs, Erik G., Louis M. Luttrell y Mi-Hye Lee. "Probing Arrestin Function Using Intramolecular FlAsH-BRET Biosensors". En Beta-Arrestins, 309–22. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9158-7_19.
Texto completoChen, Qiuyan, Ya Zhuo, Miyeon Kim, Susan M. Hanson, Derek J. Francis, Sergey A. Vishnivetskiy, Christian Altenbach, Candice S. Klug, Wayne L. Hubbell y Vsevolod V. Gurevich. "Self-Association of Arrestin Family Members". En Arrestins - Pharmacology and Therapeutic Potential, 205–23. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-41199-1_11.
Texto completoLally, Ciara C. M. y Martha E. Sommer. "Quantification of Arrestin–Rhodopsin Binding Stoichiometry". En Methods in Molecular Biology, 235–50. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2330-4_16.
Texto completoYvinec, Romain, Mohammed Akli Ayoub, Francesco De Pascali, Pascale Crépieux, Eric Reiter y Anne Poupon. "Workflow Description to Dynamically Model β-Arrestin Signaling Networks". En Beta-Arrestins, 195–215. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9158-7_13.
Texto completoLuan, Bing, Jian Zhao y Gang Pei. "Methods to Investigate β-Arrestin Function in Metabolic Regulation". En Beta-Arrestins, 365–84. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9158-7_23.
Texto completoActas de conferencias sobre el tema "?-arrestin"
Akins-Rivers, E. Joy, Nikia Smith y 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". En 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.
Texto completoLin, Rui, David A. Zidar y Julia K. L. Walker. "Beta-arrestin-2-dependent Signaling Promotes Th2 Cell CCR4-mediated Chemotaxis". En 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.
Texto completoSobolesky, Philip M., Tanyau Zhou, Arielle Gorstein, Julie A. Woolworth y Omar Moussa. "Abstract 4070: β-arrestin-2 mediated regulation of plasminogen activator inhibitor Type 1." En Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-4070.
Texto completoPillai, Smitha R., Michael Damit y Srikumar Chellappan. "Abstract 2951: Nicotine induced EMT involves β-arrestin-1 mediated regulation of E2F1 target genes". En Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-2951.
Texto completoMasannat, Jude, Yushan Zhang, Hamsa Purayil, Iqbal Mahmud y Yehia Daaka. "Abstract 1982: β-arrestin 2 mediates tumor growth and metastasis in renal cell carcinoma cells". En Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-1982.
Texto completoPillai, Smitha, Jose Trevino, Bhupendra Rawal, Sandeep Singh, Xueli Li, Michael Schell, Eric Haura, Gerold Bepler y Srikumar Chellappan. "Abstract 4993: Nicotine induced EMT and metastasis of human NSCLC : Role of beta-arrestin-1". En Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-4993.
Texto completoPera, T., E. Tompkins, D. A. Deshpande, A. P. Nayak y R. B. Penn. "Biased Regulation of OGR1 Biased Signaling in Airway Smooth Muscle Cells: GRK2/3 and Arrestin Potluck". En American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a2849.
Texto completoMowart, Tonelia A., Timothy Adekoya, Nikia Smith, Tonya S. Lane y Ricardo M. Richardson. "Abstract B005: Ginger consumption inhibits β-arrestin-2 expression and functions in melanoma and prostate cancer cells". En Abstracts: AACR Special Conference: Prostate Cancer: Advances in Basic, Translational, and Clinical Research; December 2-5, 2017; Orlando, Florida. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.prca2017-b005.
Texto completoKallifatidis, Georgios, Daniel Munoz, Rajendra K. Singh y Bal L. Lokeshwar. "Abstract 4993: β-arrestin-2 regulates CXCR7-mediated EGFR transactivation and tumor cell proliferation in prostate cancer cells". En Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-4993.
Texto completoJohnston, R. A., A. W. Pilkington, IV, M. L. Kashon y J. S. Reynolds. "β-Arrestin-1 Deficiency Reduces Airway Responsiveness to Methacholine in a Mouse Model of Irritant-Induced Occupational Asthma". En American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a4508.
Texto completoInformes sobre el tema "?-arrestin"
Civale, L., L. Krusin-Elbaum, A. D. Marwick, F. Holtzberg, C. Feild, J. R. Thompson, R. Wheeler, M. A. Kirk y Y. R. Sun. Arresting vortex motion in YBaCuO crystals with splay in columnar defects. Office of Scientific and Technical Information (OSTI), enero de 1994. http://dx.doi.org/10.2172/204571.
Texto completoClague, J. J. y 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.
Texto completoWagener, Brant M. The Role of CXCR4 and Arrestins in Breast Cancer Signaling and Apoptosis. Fort Belvoir, VA: Defense Technical Information Center, febrero de 2006. http://dx.doi.org/10.21236/ada448129.
Texto completoWagener, Brant M. The Role of CXCR4 and Arrestins in Breast Cancer Signaling and Apoptosis. Fort Belvoir, VA: Defense Technical Information Center, febrero de 2005. http://dx.doi.org/10.21236/ada434113.
Texto completoCarlson, Mark, Kris James Mitchener y Gary Richardson. Arresting Banking Panics: Fed Liquidity Provision and the Forgotten Panic of 1929. Cambridge, MA: National Bureau of Economic Research, octubre de 2010. http://dx.doi.org/10.3386/w16460.
Texto completoBly, Peter. Development of expedient ultra-high molecular weight aircraft arresting system panel installation procedures. Engineer Research and Development Center (U.S.), julio de 2020. http://dx.doi.org/10.21079/11681/37536.
Texto completoBrown, E. R. Evaluation of Ultra High Molecular Weight (UHMW) Polyethylene Panels for Aircraft Arresting Systems. Fort Belvoir, VA: Defense Technical Information Center, agosto de 2009. http://dx.doi.org/10.21236/ada508608.
Texto completoGervasio, Dominic. Sensing and arresting metal corrosion in molten chloride salts at 800 degrees Celsius. Office of Scientific and Technical Information (OSTI), julio de 2021. http://dx.doi.org/10.2172/1806305.
Texto completoPrud’homme, Joseph. Quakerism, Christian Tradition, and Secular Misconceptions: A Christian’s Thoughts on the Political Philosophy of Ihsan. IIIT, octubre de 2020. http://dx.doi.org/10.47816/01.006.20.
Texto completoSparacino, PeterL, Joseph W. Krulikowski y John F. Kenefick. The National Shipbuilding Research Program, 1990 Ship Production Symposium, Paper No. 7B-2: Photogrammetry, Shipcheck of USS Constellation (cv64) Arresting Gear Engines. Fort Belvoir, VA: Defense Technical Information Center, agosto de 1990. http://dx.doi.org/10.21236/ada451794.
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