Academic literature on the topic 'ORAOV1'
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Journal articles on the topic "ORAOV1"
Jiang, L., H. S. Yang, Z. Wang, Y. Zhou, M. Zhou, X. Zeng, and Q. M. Chen. "ORAOV1-A Correlates with Poor Differentiation in Oral Cancer." Journal of Dental Research 88, no. 5 (May 2009): 433–38. http://dx.doi.org/10.1177/0022034509336994.
Full textXavier, Flávia Caló Aquino, Camila Oliveira Rodini, Katiúcia Batista Silva Paiva, Maria Fernanda Souza Setúbal Destro, Patricia Severino, Raquel A. Moyses, Eloiza H. Tajara, and Fabio Daumas Nunes. "ORAOV1 is amplified in oral squamous cell carcinoma." Journal of Oral Pathology & Medicine 41, no. 1 (May 28, 2011): 54–60. http://dx.doi.org/10.1111/j.1600-0714.2011.01053.x.
Full textСалеева, Д. В., В. Ф. Михайлов, Л. В. Шуленина, В. В. Виноградов, А. А. Бахтин, К. В. Акопян, М. В. Незнанова, and Г. Д. Засухина. "Activities of regulatory RNAs that affect development of tumor cells in patients with laryngeal cancer." ZHurnal «Patologicheskaia fiziologiia i eksperimental`naia terapiia», no. 4() (November 21, 2018): 67–74. http://dx.doi.org/10.25557/0031-2991.2018.04.67-74.
Full textJiang, Lu, Xin Zeng, Zhi Wang, Ning Ji, Yu Zhou, Xianting Liu, and Qianming Chen. "Oral cancer overexpressed 1 (ORAOV1) regulates cell cycle and apoptosis in cervical cancer HeLa cells." Molecular Cancer 9, no. 1 (2010): 20. http://dx.doi.org/10.1186/1476-4598-9-20.
Full textTogashi, Y., T. Arao, H. Kato, K. Matsumoto, M. Terashima, H. Hayashi, Y. Fujita, T. Yasuda, H. Shiozaki, and K. Nishio. "ORAOV1 is Amplified in Esophageal Squamous Cell Cancer and Related to Tumor Growth and Poorly Differentiated Tumor." Annals of Oncology 24 (November 2013): ix60. http://dx.doi.org/10.1093/annonc/mdt459.131.
Full textPrusty, Nihar Ranjan, Francesca Camponeschi, Simone Ciofi-Baffoni, and Lucia Banci. "The human YAE1-ORAOV1 complex of the cytosolic iron-sulfur protein assembly machinery binds a [4Fe-4S] cluster." Inorganica Chimica Acta 518 (April 2021): 120252. http://dx.doi.org/10.1016/j.ica.2021.120252.
Full textSalmon Hillbertz, Nicolette H. C., Magnus Isaksson, Elinor K. Karlsson, Eva Hellmén, Gerli Rosengren Pielberg, Peter Savolainen, Claire M. Wade, et al. "Duplication of FGF3, FGF4, FGF19 and ORAOV1 causes hair ridge and predisposition to dermoid sinus in Ridgeback dogs." Nature Genetics 39, no. 11 (September 30, 2007): 1318–20. http://dx.doi.org/10.1038/ng.2007.4.
Full textZhao, Xin, Dongjuan Liu, Lili Wang, Ruiqing Wu, Xin Zeng, Hongxia Dan, Ning Ji, Lu Jiang, Yu Zhou, and Qianming Chen. "RNAi-mediated downregulation of oral cancer overexpressed 1 (ORAOV1) inhibits vascular endothelial cell proliferation, migration, invasion, and tube formation." Journal of Oral Pathology & Medicine 45, no. 4 (October 9, 2015): 256–61. http://dx.doi.org/10.1111/jop.12371.
Full textJiang, Lu, Xin Zeng, Hanshuo Yang, Zhi Wang, Jun Shen, Jingping Bai, Yuanyuan Zhang, Feng Gao, Min Zhou, and Qianming Chen. "Oral cancer overexpressed 1 (ORAOV1): A regulator for the cell growth and tumor angiogenesis in oral squamous cell carcinoma." International Journal of Cancer 123, no. 8 (October 15, 2008): 1779–86. http://dx.doi.org/10.1002/ijc.23734.
Full textTogashi, Yosuke, Tokuzo Arao, Hiroaki Kato, Kazuko Matsumoto, Masato Terashima, Hidetoshi Hayashi, Marco A. de Velasco, et al. "Frequent amplification of ORAOV1 gene in esophageal squamous cell cancer promotes an aggressive phenotype via proline metabolism and ROS production." Oncotarget 5, no. 10 (December 30, 2013): 2962–73. http://dx.doi.org/10.18632/oncotarget.1561.
Full textDissertations / Theses on the topic "ORAOV1"
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.
Full textJensen, 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.
Full textCalmodulin (CaM) plays an important role in calcium (Ca2+)-dependent signal transduction. Ca2+ binding to CaM triggers a conformational change, forming a hydrophobic patch that is important for target protein recognition. CaM regulates a Ca2+-dependent inactivation (CDI) process in store-operated Ca2+ entry (SOCE), by interacting with the N-terminus of the hexameric plasma membrane Ca2+ channel Orai1. To understand the relationship between Ca2+-induced hydrophobicity of CaM and the CaM/Orai interaction, chimera proteins constructed by exchanging EF-hands of CaM with those of Troponin C (TnC) were used as an informative probe to better understand the functionality of each EF-hand. ANS was used to assess the context of the induced hydrophobic surface on CaM and chimeras upon Ca2+ binding. The exchanged EF-hands from TnC to CaM resulted in reduced hydrophobicity compared with wild-type CaM, as depicted by ANS fluorescence and binding affinity. Such a conclusion is consistent with general concepts about the inadequacy of hydrophobic exposure for chimeras. However, such ANS responses exhibited no correlation with the ability to interact with Orai1. ANS lifetime measurements indicated that there are two types of ANS molecules with rather distinct fluorescence lifetimes, each specifically corresponding to one lobe of CaM or chimeras. Thermodynamic studies indicated the interaction between CaM and a 24-residue peptide corresponding to the CaM-binding domain of Orail1 (Orai-CMBD) is a 1:2 CaM/Orai-CMBD binding, in which each peptide binding yields a similar enthalpy change (ΔH = − 5.02 ± 0.13 kcal/mol) and binding affinity (Ka = 8.92 ± 1.03 x 105 M−1). With the exchanged EF1 and EF2, the resulting chimeras noted as CaM(1TnC) and CaM(2TnC), displayed a two sequential binding mode with a one-order weaker binding affinity and lower ?H than that of CaM, while CaM(3TnC) and CaM(4TnC) had similar binding thermodynamics as CaM. Circular Dichroism studies suggested differences in binding most likely resulted from changes in chimera three-dimensional structure rather than secondary structure, as the extent of ?-helical content from apo-, Ca2+-, and Orai-CMBD-bound proteins remained similar. The dissociation rate constant for CaM/Orai-CMBD was determined to be 1.41 ± 0.08 s−1 by rapid kinetics. Stern-Volmer plots of Orai-CMBD Trp76, indicated that the residue is located in a very hydrophobic environment but becomes more solvent accessible when EF1 and EF2 were exchanged. Here, the model of 1:2 binding stoichiometry of CaM/Orai-CMBD established in solution supports the unique, open binding mode suggested by already published structural studies.
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.
Full textBartoli, Fiona. "Le canal calcique Orai1 : nouvel acteur impliqué dans la physiopathologie cardiaque." Thesis, Université Paris-Saclay (ComUE), 2018. http://www.theses.fr/2018SACLS027.
Full textWhile the SOCE (store-operated Ca2+ entry), carried by TRPCs (transient receptor potential canonical) and Orai1 channels, is essential in non-excitable cells, its physiological role in adult cardiomyocytes remains elusive. Nevertheless, it is well established that exacerbated TRPCs/STIM1-dependent Ca2+ entry participates in the pathogenesis of hypertrophy and heart failure (HF) via the induction of pro-hypertrophic signaling pathways, such as CaMKII (Ca2+/calmodulin-kinase II) and calcineurin (CaN)/ NFAT (nuclear factor of activated T-cells). By contrast, functional inhibition or gene silencing of TRPCs and STIM1 is cardioprotective against hypertrophic insults. As for Orai1 Ca2+ channels, their pathophysiological roles in the heart remain unknown and under debate, since in vitro Orai1 silencing has a beneficial effect against cardiomyocyte hypertrophy, whereas in vivo silencing has deleterious effects with the development of dilated cardiomyopathy. Further investigations are necessary to determine the pathophysiological role of Orai1 in the heart. My thesis objectives are to explore the role of Orai1-dependent Ca2+ signaling in the heart under physiological and pathological conditions using a transgenic mouse model expressing a non functional mutant of Orai1, specifically in the heart (dn-Orai1R91W/tTa) and a selective pharmacological inhibitor, JPIII. First, we showed that dn-Orai1R91W/tTa mice have normal cardiac function and conserved Ca2+ homeostasis involved in the excitation-contraction coupling suggesting that Orai1 is not instrumental in regulating cardiac function under physiological conditions. However, we demonstrated an increased Orai1 expression and activity in a mouse model of cardiac hypertrophy induced by pressure overload, which is a maladaptive alteration involved in pathological ventricular dysfunction. By contrast, functional inhibition of Orai1 by genetic manipulation or by the pharmacological tool (JPIII) protects the heart from ventricular dysfunction after pressure overload-induced cardiac hypertrophy. This beneficial effect is related to a restoration of Ca2+ homeostasis and more specifically, is due to preserved ATPase SERCA2a pump expression. We also showed that the aldosterone/mineralocorticoid receptor signaling pathway modulates the expression of TRPC1, -C4, -C5 channels and also the Orai1 channels expression via the SGK1 (Serum and Glucocorticoid-regulated Kinase 1) protein, in neonatal rat ventricular cardiomyocytes. The activation of this signaling pathway could be the cause of the TRPCs/Orai1 channels overexpression found during cardiac hypertrophy. In conclusion, our studies highlighted that Orai1 Ca2+ channels could constitute potential therapeutic target in the treatment of cardiac hypertrophy and HF
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.
Full textAlteration in glycosylation pattern is one of the hallmarks of breast cancer. The levels and the abnormal expressions of glycan were found in breast cancer patients. Glycosylation defect can affect different glycosylated proteins which are implicated in cancerogenesis. Changes in intracellular Ca2+ levels can regulate different cellular processes. SOC channels are implicated in breast cancer proliferation, migration and survival. CO-OCS is a new glycosylation inhibitor with more selectivity toward theα- glucosidases exhibited anti-cancer activities in breast cancer cells without affecting the normal mammary cells. The objective of my thesis is investigating the related molecular mechanisms by which CO-OCS induced its anti-tumour effects.CO-OCS impaired breast cancer migration through decrease β1-integrin expression and the activation of FAK and ERK1/2 signalling pathways. CO-OCS also induced anti-migratory effect via Stim1 protein expression down-regulation leading to inhibition of SOCE. Additionally, CO-OCS affected the expression of both Orai1 and Stim1 proteins leading to anti-proliferative effects and cell cycle arrest in G1 and G2/M phase respectively. Moreover, CO-OCS affected the expression of Stim1 at the protein level without affecting its transcript level. GRP78 implicated in CO-OCS apoptotic death. The expression of Stim1 regulated the apoptosis induced by CO-OCS via modulating GRP78 expression. Orai1 down-regulation promoted CO-OCS necrotic effect. CO-OCS induced ER- calcium depletion due to increase in ER calcium leak via the Translocon; Anisomycin (Translocon inhibitor) decreased the apoptosis induced by CO-OCS. In conclusion, these results show that in breast cancer, by targeting Stim1, Orai1 and GRP78, CO-OCS reduced cell proliferation and induced apoptosis and necrosis cell death. Stim1 favours CO-OCS apoptotic effect while Orai1 protected from necrosis induced by CO-OCS. The inhibition of Translocon decreased CO-OCS apoptotic cell death via restoring the ER calcium homeostasis
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.
Full textProstate cancer (PCa) is the most frequent and the third deadliest cancer in men in Europe. Cancer stem cells (CSC) are a rare subset of cancer cells possessing stem cell properties leading to a high resistance to therapy and an enhanced tumorigenicity. As a result, CSCs have been linked to tumor dormancy and relapse upon reactivation. Thus, the mechanisms regulating CSC dormancy/activation transition are of critical importance in PCa. Previous studies showed the importance of Orai proteins in PCa, through their roles in SOC (store-operated channel) and ARC (arachidonic acid-regulated calcium channel) channels. But the role of Orai1 in PCa proliferation and CSC physiology remained to be studied. Moreover, in order to bypass current targeting limitations for Orai1, we aimed to identify a partner protein able to regulate Orai1 in PCa. For this purpose, we focused on the Sigma 1 receptor (S1R), a chaperone protein capable of ion channel regulation. Interestingly, S1R expression is increased in PCa and this protein can bind many pharmacological compounds currently used for other clinical applications. This work thus aimed to first study the role of Orai1 in PCa and CSC physiology, and then characterize the role of S1R as a new regulator of Orai1 in PCa. Our results first show that Orai1 is a key regulator of CSC transition between quiescence and proliferation via the NFAT pathway. Moreover, this role is not limited to PCa, since these results were also confirmed in melanoma CSCs. We also show here that the S1R directly interacts with Orai1 and increases its activity, thus modulating PCa cell proliferation. Finally, we characterized the regulation of Orai1 and S1R expression by androgens, which is highly significant during PCa development. Our results therefore allowed the identification of a key regulator of PCa proliferation (Orai1), and propose an alternative method for its targeting via the identification of its partner protein (S1R). These results could lead to the development of new markers and innovative therapeutic strategies
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.
Full textWe showed that a K+ channel, SK3 channel, is a mediator of MDA-MB-435s breast cancer cells migration and of osteolytic bone metastasis development of breast cancer. Since [Ca²+]out rises during osteolysis, in bone microenvironment, we study if this [Ca²+]out elevation could modulate SK3 expression and activity. We show that [Ca²+]out elevation: i) increases SK3 expression threw CaSR activation which, in turn, decreases [cAMP]int and PKA activation, leading to loss of its inhibitory effect on KCNN3 transcription; ii) increases SK3-dependent migration threw CaSR activation; iii) increases SK3 channel activity that is in addition, decreased by [cAMP]int elevation. Furthermore, cAMP elevation moves the Ca2+ channel Orai1 (SK3 partner) outside of lipid rafts and reduces the SK3 dependent-constitutive Ca²+ entry and cell migration. Our results show that both SK3 expression and activity are regulated by cAMP and extracellular Ca²+. These results underscore an innovative opportunity to use therapeutic approaches targeting cAMP for the treatment of breast cancer bone metastasis
Hassan, S. Faisal (Syed Faisal). "Pan-Orao and historical necessity : adjusted frames and optical settlement." Thesis, Massachusetts Institute of Technology, 1995. http://hdl.handle.net/1721.1/66769.
Full textIncludes bibliographical references (leaves 79-84).
Large horizontally formatted images have frequently been preferred for urban portraiture. Totalizing and comprehensive such compositions depict an environment as landscape or prospect. In rendering an all-encompassing view they attempt an expansive topographic virtuality that warrants participation. As a fictive world modeled on a surface they allow the perceiving faculties to enter places where our bodies cannot follow. By securing and seaming the edges of multiple frames, by engaging peripheral vision, they extend the limits of normal vision. This thesis has chosen to study such images giving them the title Pan Orao. By considering them a phenomenon it invests them partially the status of a mode of expression and at same time acknowledges their role as apparatus. The latter also suggests that they serve as mechanical requisites, as machinery for viewing the expansive condition of urban portraiture. The research cuts are taken across boundaries of place, time, medium and type to speak of unbroken views or serial images passing before the mind and the eye. Distinctions of 'high' and 'low' old and new therefore are not entertained. Rather a wider scaffold is suggested. The project sustains two broad conceptual themes; immersion and mobility, which are used to organise the material which ranges from Wide Screen 3D Cinema to 17th century urban views. Detailed discussion of particular cases occurs with a simultaneous interest in the technology of the changing view, its sociological and cultural impact, and the spatial-visual component of the media and their role in providing immersive environments.
by S. Faisal Hassan.
M.S.
Röther, Jens [Verfasser], Ulrich [Akademischer Betreuer] Sack, Stefan [Akademischer Betreuer] Feske, and bekannt nicht bekannt [Gutachter] nicht. "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 / Jens Röther ; Gutachter: nicht bekannt nicht bekannt ; Ulrich Sack, Stefan Feske." Leipzig : Universitätsbibliothek Leipzig, 2011. http://d-nb.info/1237894638/34.
Full textGiachini, 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/.
Full textDisturbance in the regulation of cytoplasmic calcium (Ca2+) concentration contributes to the pathogenesis of hypertension. Evidences suggest that the stromal interaction molecule (STIM) acts as a sensor of intracellular Ca2+ stores, whereas Orai proteins are the subunits that form CRAC channels. In this study, we evaluated the role of STIM1/Orai1 in the regulation of cytoplasmic Ca2+ concentrations and in the activation of contraction in aortas from hypertensive rats. We also studied how the differential activation of this pathway contributes to sex differences observed between hypertensive rats, as well as the protective effects of the female sex hormones in the vasculature. Our results suggest that activation of STIM1/Orai1 may represent a new mechanism that modulates intracellular Ca2+ concentration during hypertension and contributes to sex differences in the vascular reactivity of hypertensive animals.
Books on the topic "ORAOV1"
Orahova ljuska. Beograd: Čigoja štampa, 2003.
Find full textBochow, Karl-Heinz. Orava. Leipzig: Brockhaus, 1990.
Find full textSijarić, Ćamil. Miris lišća orahova. Sarajevo: Preporod, 2004.
Find full textPeter, Huba, and Mikláš Milan, eds. Premeny Oravy. Martin: Vyd. Osveta, 1985.
Find full textauthor, Urām̐va Becana 1975, and Tribhuvana Viśvavidyālaya. Central Department of Sociology and Anthropology, eds. Oraon of Nepal. Kathmandu, Nepal: Central Department of Sociology/Anthropology, Tribhuvan University, 2014.
Find full textBenović, Ljubica. Kliješta za razbijanje orahove ljuske. Grude: Ogranak matice hrvatske Grude, 2006.
Find full textKliješta za razbijanje orahove ljuske. Grude: Ogranak matice hrvatske Grude, 2006.
Find full textMatovcik, Augustin. Hviezdoslav a rodna Orava. Martin: Matica slovenska, 1999.
Find full textLanger, Juraj. Cesty po minulosti Oravy. [Slovakia]: Peter Huba, 1993.
Find full textOrav, Maie. Maie Orava tantsud II. Rakvere: Tarvanpää Selts, 2003.
Find full textBook chapters on the topic "ORAOV1"
Ghosh, Abhik. "Religion of the Oraons." In Hinduism and Tribal Religions, 1303–8. Dordrecht: Springer Netherlands, 2022. http://dx.doi.org/10.1007/978-94-024-1188-1_842.
Full textGhosh, Abhik. "Religion of the Oraons." In Hinduism and Tribal Religions, 1–6. Dordrecht: Springer Netherlands, 2021. http://dx.doi.org/10.1007/978-94-024-1036-5_842-1.
Full textYee, Christina. "Calcium Channel Defects (STIM1 and ORAI1)." In Encyclopedia of Medical Immunology, 86–91. New York, NY: Springer New York, 2020. http://dx.doi.org/10.1007/978-1-4614-8678-7_176.
Full textYee, Christina. "Calcium Channel Defects (STIM1 and ORAI1)." In Encyclopedia of Medical Immunology, 1–6. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4614-9209-2_176-1.
Full textBandia, Paul. "Orality and translation." In Handbook of Translation Studies, 108–12. Amsterdam: John Benjamins Publishing Company, 2011. http://dx.doi.org/10.1075/hts.2.ora1.
Full textDerler, Isabella, Josef Madl, Gerhard Schütz, and Christoph Romanin. "Structure, Regulation and Biophysics of ICRAC, STIM/Orai1." In Advances in Experimental Medicine and Biology, 383–410. Dordrecht: Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-94-007-2888-2_16.
Full textWoo, Jin Seok, Sonal Srikanth, and Yousang Gwack. "Modulation of Orai1 and STIM1 by Cellular Factors." In Calcium Entry Channels in Non-Excitable Cells, 73–92. Boca Raton : Taylor & Francis, 2017. | Series: Methods in signal transduction series: CRC Press, 2017. http://dx.doi.org/10.1201/9781315152592-4.
Full textCheng, 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, 435–49. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-94-007-0265-3_24.
Full textZhou, 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, 127–44. Boca Raton : Taylor & Francis, 2017. | Series: Methods in signal transduction series: CRC Press, 2017. http://dx.doi.org/10.1201/9781315152592-7.
Full textCioffi, 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, 137–54. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60761-500-2_9.
Full textConference papers on the topic "ORAOV1"
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.
Full textHubrack, 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.
Full textAhmad, 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.
Full textMasson, Bastien, Hélène Le Ribeuz, Jessica Sabourin, Emily Woodhouse, Richard Foster, Yann Ruchon, Mary Dutheil, 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.
Full textPelzl, L., I. Sahu, D. Heinzmann, A. A. M. Bhuyan, T. a. Maghout, I. Marini, F. Rigoni, 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.
Full textLatour, 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.
Full textDib, 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.
Full textTarran, 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.
Full textYang, 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.
Full textHodeify, Rawad, Senthil Selvaraj, Jennifer Wen, Abdelilah Arredoouani, Satanay Hubrack, Sara Al-thani, Timothy Mcgraw, and Khaled Machaca. "Molecular Determinants Of The Store-operated Ca2+ Entry Channel Orai1 Trafficking In Mammalian Cells." In Qatar Foundation Annual Research Conference Proceedings. Hamad bin Khalifa University Press (HBKU Press), 2014. http://dx.doi.org/10.5339/qfarc.2014.hbpp0160.
Full textReports on the topic "ORAOV1"
Huang, Xin-Yun. Orai1 as New Therapeutic Target for Inhibiting Breast Tumor Metastasis. Fort Belvoir, VA: Defense Technical Information Center, September 2009. http://dx.doi.org/10.21236/ada518249.
Full text