Relevant bibliographies by topics / Orai1

Contents

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

Academic literature on the topic 'Orai1'

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

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Journal articles on the topic "Orai1"

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Eckstein, Miriam, Martin Vaeth, Francisco J. Aulestia, et al. "Differential regulation of Ca2+ influx by ORAI channels mediates enamel mineralization." Science Signaling 12, no. 578 (2019): eaav4663. http://dx.doi.org/10.1126/scisignal.aav4663.

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Store-operated Ca2+ entry (SOCE) channels are highly selective Ca2+ channels activated by the endoplasmic reticulum (ER) sensors STIM1 and STIM2. Their direct interaction with the pore-forming plasma membrane ORAI proteins (ORAI1, ORAI2, and ORAI3) leads to sustained Ca2+ fluxes that are critical for many cellular functions. Mutations in the human ORAI1 gene result in immunodeficiency, anhidrotic ectodermal dysplasia, and enamel defects. In our investigation of the role of ORAI proteins in enamel, we identified enamel defects in a patient with an ORAI1 null mutation. Targeted deletion of the O
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Jardin, Isaac, Alejandro Berna-Erro, Joel Nieto-Felipe та ін. "Similarities and Differences between the Orai1 Variants: Orai1α and Orai1β". International Journal of Molecular Sciences 23, № 23 (2022): 14568. http://dx.doi.org/10.3390/ijms232314568.

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Orai1, the first identified member of the Orai protein family, is ubiquitously expressed in the animal kingdom. Orai1 was initially characterized as the channel responsible for the store-operated calcium entry (SOCE), a major mechanism that allows cytosolic calcium concentration increments upon receptor-mediated IP3 generation, which results in intracellular Ca2+ store depletion. Furthermore, current evidence supports that abnormal Orai1 expression or function underlies several disorders. Orai1 is, together with STIM1, the key element of SOCE, conducting the Ca2+ release-activated Ca2+ (CRAC)
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Liang, Ch, and F. Wu. "Reconstitution of calcium channel protein Orai3 into liposomes for functional studies." Биохимия 88, no. 9 (2023): 1570–80. http://dx.doi.org/10.31857/s0320972523090099.

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Store-operated calcium entry (SOCE) is the main mechanism for the Ca2+ influx in non-excitable cells. The two major components of SOCE are stromal interaction molecule 1 (STIM1) in the endoplasmic reticulum and Ca2+ release-activated Ca2+ channel (CRAC) Orai on the plasma membrane. SOCE requires interaction between STIM1 and Orai. Mammals have three Orai homologs: Orai1, Orai2, and Orai3. Although Orai1 has been widely studied and proven to be essential for numerous cellular processes, Orai3 has also attracted a significant attention recently. The gating and activation mechanisms of Orai3 have
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Fresquez, Adriana M., and Carl White. "Extracellular cysteines C226 and C232 mediate hydrogen sulfide-dependent inhibition of Orai3-mediated store-operated calcium entry." American Journal of Physiology-Cell Physiology 322, no. 1 (2022): C38—C48. http://dx.doi.org/10.1152/ajpcell.00490.2019.

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The gaseous signaling molecule hydrogen sulfide (H2S) physiologically regulates store-operated Ca2+ entry (SOCE). The SOCE machinery consists of the plasma membrane-localized Orai channels (Orai1-3) and endoplasmic reticulum-localized stromal interaction molecule (STIM)1 and STIM2 proteins. H2S inhibits Orai3- but not Orai1- or Orai2-mediated SOCE. The current objective was to define the mechanism by which H2S selectively modifies Orai3. We measured SOCE and STIM1/Orai3 dynamics and interactions in HEK293 cells exogenously expressing fluorescently tagged human STIM1 and Orai3 in the presence a
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Grimes, Derayvia, Ryan Johnson, Madeline Pashos, et al. "ORAI1 and ORAI2 modulate murine neutrophil calcium signaling, cellular activation, and host defense." Proceedings of the National Academy of Sciences 117, no. 39 (2020): 24403–14. http://dx.doi.org/10.1073/pnas.2008032117.

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Calcium signals are initiated in immune cells by the process of store-operated calcium entry (SOCE), where receptor activation triggers transient calcium release from the endoplasmic reticulum, followed by opening of plasma-membrane calcium-release activated calcium (CRAC) channels. ORAI1, ORAI2, and ORAI3 are known to comprise the CRAC channel; however, the contributions of individual isoforms to neutrophil function are not well understood. Here, we show that loss of ORAI1 partially decreases calcium influx, while loss of both ORAI1 and ORAI2 completely abolishes SOCE. In other immune-cell ty
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Smyth, Jeremy T., and James W. Putney. "Regulation of store-operated calcium entry during cell division." Biochemical Society Transactions 40, no. 1 (2012): 119–23. http://dx.doi.org/10.1042/bst20110612.

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Store-operate Ca2+ channels gate Ca2+ entry into the cytoplasm in response to the depletion of Ca2+ from endoplasmic reticulum Ca2+ stores. The major molecular components of store-operated Ca2+ entry are STIM (stromal-interacting molecule) 1 (and in some instances STIM2) that serves as the endoplasmic reticulum Ca2+ sensor, and Orai (Orai1, Orai2 and Orai3) which function as pore-forming subunits of the store-operated channel. It has been known for some time that store-operated Ca2+ entry is shut down during cell division. Recent work has revealed complex mechanisms regulating the functions an
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Tiffner, Adéla, and Isabella Derler. "Isoform-Specific Properties of Orai Homologues in Activation, Downstream Signaling, Physiology and Pathophysiology." International Journal of Molecular Sciences 22, no. 15 (2021): 8020. http://dx.doi.org/10.3390/ijms22158020.

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Ca2+ ion channels are critical in a variety of physiological events, including cell growth, differentiation, gene transcription and apoptosis. One such essential entry pathway for calcium into the cell is the Ca2+ release-activated Ca2+ (CRAC) channel. It consists of the Ca2+ sensing protein, stromal interaction molecule 1 (STIM1) located in the endoplasmic reticulum (ER) and a Ca2+ ion channel Orai in the plasma membrane. The Orai channel family includes three homologues Orai1, Orai2 and Orai3. While Orai1 is the “classical” Ca2+ ion channel within the CRAC channel complex and plays a univers
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Zhang, Xuexin, Ping Xin, Ryan E. Yoast, et al. "Distinct pharmacological profiles of ORAI1, ORAI2, and ORAI3 channels." Cell Calcium 91 (November 2020): 102281. http://dx.doi.org/10.1016/j.ceca.2020.102281.

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Baryshnikov, Sergey G., Maria V. Pulina, Alessandra Zulian, Cristina I. Linde, and Vera A. Golovina. "Orai1, a critical component of store-operated Ca2+ entry, is functionally associated with Na+/Ca2+ exchanger and plasma membrane Ca2+ pump in proliferating human arterial myocytes." American Journal of Physiology-Cell Physiology 297, no. 5 (2009): C1103—C1112. http://dx.doi.org/10.1152/ajpcell.00283.2009.

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Ca2+ entry through store-operated channels (SOCs) in the plasma membrane plays an important role in regulation of vascular smooth muscle contraction, tone, and cell proliferation. The C-type transient receptor potential (TRPC) channels have been proposed as major candidates for SOCs in vascular smooth muscle. Recently, two families of transmembrane proteins, Orai [also known as Ca2+ release-activated Ca2+ channel modulator (CRACM)] and stromal interacting molecule 1 (STIM1), were shown to be essential for the activation of SOCs mainly in nonexcitable cells. Here, using small interfering RNA, w
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Liu, Xiaoling, Tianyuan Zheng, Yan Jiang, et al. "Molecular Mechanism Analysis of STIM1 Thermal Sensation." Cells 12, no. 22 (2023): 2613. http://dx.doi.org/10.3390/cells12222613.

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STIM1 has been identified as a new warm sensor, but the exact molecular mechanism remains unclear. In this study, a variety of mutants of STIM1, Orai1 and Orai3 were generated. The single–cell calcium imaging and confocal analysis were used to evaluate the thermal sensitivity of the resulting STIM mutants and the interaction between STIM1 and Orai mutants in response to temperature. Our results suggested that the CC1–SOAR of STIM1 was a direct activation domain of temperature, leading to subsequent STIM1 activation, and the transmembrane (TM) region and K domain but not EF–SAM were needed for
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Dissertations / Theses on the topic "Orai1"

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Röther, Jens. "Die Rolle von Orai1 in der Entwicklung und Aktivierung von T- und B- Lymphozyten und die Bedeutung von Mutationen in Orai1 für die Pathogenese schwerer kombinierter Immundefekte." Doctoral thesis, Universitätsbibliothek Leipzig, 2011. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-70949.

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Ein durch „Ca2+ Release Activated Ca2+ (CRAC)“-Kanal vermittelter Ca2+-Einstrom ist unverzichtbar für die vollständige Aktivierung von T-Zellen und eine produktive Immunantwort. Im Jahr 2006 führte die Entdeckung des transmembranen Proteins Orai1, einer porenbildenden Untereinheit des CRAC-Kanals, zu einem besseren Verständnis dieses Signalweges. Eine Mutation in Orai1 hat durch die Aufhebung der CRAC-Kanal Funktion eine schwere kombinierte Immundefizienz (SCID) zur Folge (Feske, S. et al. 2006). Die im Rahmen dieser Arbeit präsentierten Experimente hatten die nähere Erforschung der Rolle von
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Jensen, Drake. "Functional Analysis of Calmodulin's Calcium Dependent Inactivation of Orai1." Thesis, Southern Illinois University at Edwardsville, 2015. http://pqdtopen.proquest.com/#viewpdf?dispub=1589551.

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<p> Calmodulin (CaM) plays an important role in calcium (Ca<sup>2+</sup>)-dependent signal transduction. Ca<sup>2+</sup> binding to CaM triggers a conformational change, forming a hydrophobic patch that is important for target protein recognition. CaM regulates a Ca<sup>2+</sup>-dependent inactivation (CDI) process in store-operated Ca<sup>2+</sup> entry (SOCE), by interacting with the N-terminus of the hexameric plasma membrane Ca<sup>2+</sup> channel Orai1. To understand the relationship between Ca<sup>2+</sup>-induced hydrophobicity of CaM and the CaM/Orai interaction, chimera proteins cons
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Gueder, Nahla. "sp²-Iminosugar-glucosidases inhibitor 1-C-octyl-2-oxa-3-oxocastanospermine - induced antiproliferative, apoptotic and necrotic effects in breast cancer cells via targeting GRP78, Stim1 and Orai1." Thesis, Amiens, 2018. http://www.theses.fr/2018AMIE0033/document.

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L'altération de glycosylation est l'une des caractéristiques du cancer du sein. Ainsi le défaut de glycosylation affecte différentes protéines glycosylées responsables des différents processus cancéreux. Les canaux SOC (Store operated channels) constituent la voie majeure de l'entrée du calcium dans les cellules et sont impliqués dans la prolifération, la migration et la survie des cellules cancéreuses du sein. CO-OCS est un nouvel inhibiteur de la glycosylation avec plus de sélectivité vis-à-vis des α-glucosidases, et montre des activités anticancéreuses des cellules cancéreuses du sein, sans
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Bartoli, Fiona. "Le canal calcique Orai1 : nouvel acteur impliqué dans la physiopathologie cardiaque." Thesis, Université Paris-Saclay (ComUE), 2018. http://www.theses.fr/2018SACLS027.

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Alors que l’entrée SOC (store-operated Ca2+ entry) portée par les canaux calciques TRPCs (transient receptor potential canonical) et Orai1 est essentielle dans les cellules non-excitables, son rôle physiologique dans les cardiomyocytes adultes reste à élucider. Néanmoins, il est largement admis qu’une entrée SOC exacerbée dépendante des canaux TRPCs et de la protéine régulatrice STIM1 participe à la pathogenèse de l’hypertrophie et de l’insuffisance cardiaque (IC) par induction de voies pro-hypertrophiques telles que la CaMKII (Ca2+/calmoduline-dépendante kinase II ) et la calcineurine (CaN)/N
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Lur, Gyorgy. "STIM1, Orai1 and store operated calcium entry in pancreatic acinar cells." Thesis, University of Liverpool, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.539501.

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Clarysse, Lucie. "Régulation du canal SK3 par l'AMPc et le calcium extracellulaire dans les cellules cancéreuses du sein." Thesis, Tours, 2013. http://www.theses.fr/2013TOUR3312/document.

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Nous avons montré un rôle d’un canal K+, le canal SK3, dans la migration des cellules cancéreuses de sein MDA-MB-435s et le développement de métastases ostéolytiques du cancer du sein. Lors de l’ostéolyse, la [Ca²+]ext augmente dans le microenvironnement osseux. Nous avons voulu déterminer si cette élévation de [Ca²+]ext, pouvait moduler l’expression et l’activité du canal SK3. Nous avons montré que l’augmentation de la [Ca²+]ext: i) favorise l’expression du canal SK3. Cet effet fait intervenir le récepteur au calcium (CaSR), qui en diminuant la [AMPc]int réduit l’activité de la PKA et lève ai
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Noyer, Lucile. "Role of Orai1 in prostate cancer proliferation and cancer stem cell quiescence/activation transition." Thesis, Lille 1, 2019. http://www.theses.fr/2019LIL1S111.

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Le cancer de la prostate (CaP) est le cancer le plus fréquent et le troisième plus mortel chez l’homme en Europe. Les cellules souches cancéreuses (CSC) représentent une sous population de cellules cancéreuses possédant des propriétés de cellules souches qui les rendent résistantes aux thérapies et hautement tumorigènes. Les CSCs sont ainsi associées aux phénomènes de dormance tumorale, puis de rechute suite à leur réactivation. Les mécanismes régulant la transition dormance/prolifération constituent donc une question centrale dans la prise en charge du cancer. L’importance des protéines Orai
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Giachini, Fernanda Regina Casagrande. "Contribuição da via STIM1/Orai1 para as diferenças relacionadas ao sexo na entrada de cálcio em miócitos vasculares durante a hipertensão arterial." Universidade de São Paulo, 2010. http://www.teses.usp.br/teses/disponiveis/42/42136/tde-28092010-170302/.

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Os distúrbios na regulação da concentração de cálcio (Ca2+) citoplasmático contribuem para a patogênese da hipertensão arterial. Evidências sugerem que as moléculas de interação estromal (STIM) atuam como sensores dos estoques intracelulares de Ca2+, enquanto as proteínas Orai representam as subunidades que formam os canais de Ca2+ ativados pela liberação de Ca2+ (CRAC). Neste estudo avaliamos a participação de STIM1/Orai1 na regulação das concentrações de Ca2+ citoplasmático e na ativação da contração vascular em aortas de ratos hipertensos. Nossos resultados sugerem que a ativação de STIM1/O
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Zanotto, Camila Ziliotto. "Papel da O-glicosilação com N-acetil-glucosamina (O-GlcNAc) no influxo e recaptação de cálcio pelo retículo sarcoplasmático em aorta de ratos: análise funcional." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/17/17133/tde-09092013-133940/.

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A O-glicosilação com N-acetil-glucosamina (O-GlcNAc) é uma modificação pós-translacional altamente dinâmica que modula diversas vias de sinalização. O processo de O-GlcNAc é controlado por duas enzimas: a enzima OGT é responsável por catalisar a adição de N-acetil-glucosamina no grupo hidroxila dos resíduos de serina e treonina, enquanto a OGA catalisa a remoção de O-GlcNAc das proteínas modificadas. Proteínas com importante papel na função vascular são alvo de O-GlcNAc e o aumento da expressão de proteínas modificadas por O-GlcNAc promove aumento da reatividade vascular para estímulos contrát
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Cabanas, Hélène. "Rôle de la signalisation calcique dans la leucémie myéloïde chronique." Thesis, Poitiers, 2016. http://www.theses.fr/2016POIT2302/document.

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La Leucémie Myéloïde Chronique (LMC) est une maladie clonale caractérisée par la présence du chromosome Philadelphie codant pour Bcr-Abl, une tyrosine kinase constitutivement active responsable de la leucémogenèse. Bien que très efficaces, les inhibiteurs de tyrosine kinase (ITKs) restent cependant inactifs sur les cellules souches leucémiques. Ce travail de thèse montre que la signalisation calcique, connue pour réguler de nombreux processus dans les cellules saines et cancéreuses, est importante dans la signalisation cellulaire au décours de la LMC. Le rôle des entrées calciques dépendantes
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Books on the topic "Orai1"

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Arquivo Público do Distrito Federal (Distrito Federal, Brazil), ed. Depoimentos orais: Catálogo. 2nd ed. Arquivo Público do Distrito Federal, 2008.

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Arquivo Público do Distrito Federal (Distrito Federal, Brazil), ed. Depoimentos orais: Catálogo. 2nd ed. Arquivo Público do Distrito Federal, 2008.

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1930-, Preti Dino, Rodrigues Angela C. S, and Projeto de Estudo da Norma Lingüística Urbana Culta de São Paulo., eds. Análise de textos orais. FFLCH/USP, 1993.

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1930-, Preti Dino, Rodrigues Angela C. S, and Projeto de Estudo da Norma Lingüística Urbana Culta de São Paulo., eds. Análise de textos orais. FFLCH/USP, 1993.

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Arquivo Público do Distrito Federal (Distrito Federal, Brazil), ed. Catálogo de depoimentos orais. O Arquivo, 1994.

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S, Rodrigues Angela C., Preti Dino 1930-, and Projeto de Estudo da Norma Lingüística Urbana Culta de São Paulo., eds. Análise de textos orais. 4th ed. Humanitas Publicações, FFLCH/USP, 1999.

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Rodrigues, Angela C. S., and Dino Preti. Análise de textos orais. 7th ed. Humanitas, 2010.

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Arrayet, Eduardo. Giza migrazioak lehen eta orain. Gaiak Argitaldaria, 2007.

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Fred, Macaulay, ed. Dòmhnall Ruadh Chorùna: Orain is dain. Comann Eachdraidh Uibhist a Tuath, 1995.

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Bajoras, Vytautas. Orai: Virš Klaipėdos giedras dangus. Eglė, 2006.

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Book chapters on the topic "Orai1"

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Yee, Christina. "Calcium Channel Defects (STIM1 and ORAI1)." In Encyclopedia of Medical Immunology. Springer New York, 2020. http://dx.doi.org/10.1007/978-1-4614-8678-7_176.

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Yee, Christina. "Calcium Channel Defects (STIM1 and ORAI1)." In Encyclopedia of Medical Immunology. Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4614-9209-2_176-1.

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Derler, Isabella, Josef Madl, Gerhard Schütz, and Christoph Romanin. "Structure, Regulation and Biophysics of ICRAC, STIM/Orai1." In Advances in Experimental Medicine and Biology. Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-94-007-2888-2_16.

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Woo, Jin Seok, Sonal Srikanth, and Yousang Gwack. "Modulation of Orai1 and STIM1 by Cellular Factors." In Calcium Entry Channels in Non-Excitable Cells. CRC Press, 2017. http://dx.doi.org/10.1201/9781315152592-4.

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Cheng, Kwong Tai, Hwei Ling Ong, Xibao Liu, and Indu S. Ambudkar. "Contribution of TRPC1 and Orai1 to Ca2+ Entry Activated by Store Depletion." In Transient Receptor Potential Channels. Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-94-007-0265-3_24.

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Zhou, Yandong, Youjun Wang, and Donald L. Gill. "Assessing the Molecular Nature of the STIM1/Orai1 Coupling Interface Using FRET Approaches." In Calcium Entry Channels in Non-Excitable Cells. CRC Press, 2017. http://dx.doi.org/10.1201/9781315152592-7.

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Cioffi, Donna L., Christina Barry, and Troy Stevens. "Store-Operated Calcium Entry Channels in Pulmonary Endothelium: The Emerging Story of TRPCS and Orai1." In Advances in Experimental Medicine and Biology. Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60761-500-2_9.

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Pacheco, Jonathan, A. Bohórquez-Hernández, Kevin M. Méndez-Acevedo, Alicia Sampieri, and Luis Vaca. "Roles of Cholesterol and PtdIns(4,5)P2 in the Regulation of STIM1–Orai1 Channel Function." In Advances in Experimental Medicine and Biology. Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-21547-6_11.

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Salido, Gines M., Isaac Jardín, and Juan A. Rosado. "The TRPC Ion Channels: Association with Orai1 and STIM1 Proteins and Participation in Capacitative and Non-capacitative Calcium Entry." In Transient Receptor Potential Channels. Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-94-007-0265-3_23.

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Bartoli, Fiona, and Jessica Sabourin. "Cardiac Remodeling and Disease: Current Understanding of STIM1/Orai1-Mediated Store-Operated Ca2+ Entry in Cardiac Function and Pathology." In Store-Operated Ca²⁺ Entry (SOCE) Pathways. Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-57732-6_26.

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Conference papers on the topic "Orai1"

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Hubrack, Satanay, Ethel Adap, Stefan Feske, and Khaled Machaca. "Role Of Stim1 And Orai1 In Mammalian Oocyte Activation." In Qatar Foundation Annual Research Conference Proceedings. Hamad bin Khalifa University Press (HBKU Press), 2014. http://dx.doi.org/10.5339/qfarc.2014.hbpp0176.

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Hubrack, Satanay Zuhair, Awab Ibrahim, and Khaled Machaca. "Study of the Effect of Calreticulin on Orai1 Function." In Qatar Foundation Annual Research Conference Proceedings. Hamad bin Khalifa University Press (HBKU Press), 2016. http://dx.doi.org/10.5339/qfarc.2016.hbpp1846.

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Ahmad, S., J. Wrennall, M. Sassano, and R. Tarran. "ELD607, a Novel Anti-Orai1 Peptide Reduces Pulmonary Inflammation." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a1248.

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Masson, Bastien, Hélène Le Ribeuz, Jessica Sabourin, et al. "Late Breaking Abstract - Involvement of Orai1 Ca2+ channel in the pathogenesis of pulmonary arterial hypertension. Orai1 as a new potential therapeutic target ?" In ERS International Congress 2021 abstracts. European Respiratory Society, 2021. http://dx.doi.org/10.1183/13993003.congress-2021.pa599.

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Pelzl, L., I. Sahu, D. Heinzmann, et al. "Phosphate-induced ORAI1 Expression and Store Operated Ca2+ Entry in Megakaryocytes." In 63rd Annual Meeting of the Society of Thrombosis and Haemostasis Research. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1680097.

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Latour, Simon, Isabelle Mahouche, Floriane Cherrier, Jean-Philippe Merlio, Sandrine Poglio, and Laurence Bresson Bepoldin. "Abstract 1881: STIM1 and Orai1 control non-Hodgkin lymphoma cells migration." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-1881.

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Ahmad, S., M. Biggart, F. Sassano, A. Ghosh та R. Tarran. "The Orai1 Antagonist, ELD607, Reduces Chronic Neutrophilic Inflammation in βENaC Mice". У American Thoracic Society 2024 International Conference, May 17-22, 2024 - San Diego, CA. American Thoracic Society, 2024. http://dx.doi.org/10.1164/ajrccm-conference.2024.209.1_meetingabstracts.a6682.

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Dib, Maya, Rawad Hodeify, and Khaled Machaca. "Identification Of Proteins Involved In Orai1 Trafficking By Mass Spectrometry-based Approach." In Qatar Foundation Annual Research Conference Proceedings. Hamad bin Khalifa University Press (HBKU Press), 2014. http://dx.doi.org/10.5339/qfarc.2014.hbpp048.

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Tarran, R., S. Ahmad, J. Wrennal, E. N. Worthington, and M. F. Sassano. "Local Orai1 Inhibition Reduces Pulmonary Inflammation in House Dust Mite-Exposed Mice." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a7422.

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Yang, Shengyu, Jianwei Sun, and Huifang He. "Abstract 4317: Stim1 and Orai1 are critical regulators of melanoma invasion and anoikis." 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.am2012-4317.

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Reports on the topic "Orai1"

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Huang, Xin-Yun. Orai1 as New Therapeutic Target for Inhibiting Breast Tumor Metastasis. Defense Technical Information Center, 2009. http://dx.doi.org/10.21236/ada518249.

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Canto, Patricia, ed. Euskal Autonomia Erkidegoko Lehiakortasunari buruzko 2021eko Txostena. Ongizatea helburu duen lehiakortasuna eraikitzea. Universidad de Deusto, 2021. http://dx.doi.org/10.18543/zemz8571.

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Txosten honek, EAEko lehiakortasunaren azterketan etapa berri bat hastendu. 1. kapituluan, gure lurraldearen lehiakortasun ibilbidea aztertu dugu, orain dela 40 urte abian jarri zen estrategiak azken hamarkadan izan dituen ezaugarriei erreparatuta bereziki. Estrategia horrekin jarraitzeak gaur egun ekartzen dizkigun erronkak ere identifikatu ditugu. Estrategiaren hurrengo etapa bideratzeko, erronka horietatik abiatu gara eta, 2. kapituluan, lurralde lehiakortasuna bultzatzeko esparru berri bat proposatu dugu, tokian bertan eta nazioartean egindako gogoeta, alderatze eta esperimentazio prozesu
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Schmidt-Sane, Megan, and Tabitha Hrynick. Guia de Orientação Sobre o Envolvimento da Comunidade na Resposta a Surtos de Cólera na Região da Africa Oriental e Austral. Institute of Development Studies, 2023. http://dx.doi.org/10.19088/sshap.2023.009.

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Os surtos de cólera têm vindo a aumentar na Região da África Oriental e Austral (AOA) desde Janeiro de 2023, com uma transmissão generalizada e alargada no Malawi e em Moçambique e surtos registados na Tanzânia, na África do Sul, no Zimbabué, no Burundi e na Zâmbia.1 Existe o risco de uma maior propagação causada pelos efeitos do ciclone Freddy, que atingiu Madagáscar, o Malawi e Moçambique em Março de 2023. Continuam a registar-se surtos na Somália, na Etiópia, no Quénia e no Sudão do Sul, onde os países estão a atravessar uma situação de seca após sucessivas estações chuvosas deficitárias.1
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Nazioen Lehiatzeko Abantaila: Esperientzia arrakastatsua, Euskal Autonomia Erkidegoaren ekonomia eta gizarte garapenerako estrategia eraldatzailea bideratzekona. Universidad de Deusto, 2015. http://dx.doi.org/10.18543/pdmc8484.

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Ekonomia berriak eta ongizate gizarteek zergatik gomendatuko lukete geraleku berri bat jartzea lehiakortasunerako bidaia luzean, duela 25 urte argitaratu zen "nazioen lehiatzeko abantailaren" ildotik? Orain dela hogeita bost urte baino gehixeago, Euskal Autonomia Erkidegoak garapenerako bere estrategia eraikitzearen aldeko apustua egin zuen eta bere etorkizuna diseinatzeko erronkarekin konpromisoa hartu. Euskal Autonomia Erkidegoak ahalik eta autogobernu mailarik handiena eskuratu nahi zuen, Estaturik gabeko nazio izanik, diktadura luzetik atera ostean. Hain zuzen ere, diktadurak Espainiako ek
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