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Artykuły w czasopismach na temat "Orai1"
Eckstein, Miriam, Martin Vaeth, Francisco J. Aulestia, Veronica Costiniti, Serena N. Kassam, Timothy G. Bromage, Pal Pedersen i in. "Differential regulation of Ca2+ influx by ORAI channels mediates enamel mineralization". Science Signaling 12, nr 578 (23.04.2019): eaav4663. http://dx.doi.org/10.1126/scisignal.aav4663.
Pełny tekst źródłaJardin, Isaac, Alejandro Berna-Erro, Joel Nieto-Felipe, Alvaro Macias, Jose Sanchez-Collado, Jose J. Lopez, Gines M. Salido i Juan A. Rosado. "Similarities and Differences between the Orai1 Variants: Orai1α and Orai1β". International Journal of Molecular Sciences 23, nr 23 (23.11.2022): 14568. http://dx.doi.org/10.3390/ijms232314568.
Pełny tekst źródłaLiang, Ch, i F. Wu. "Reconstitution of calcium channel protein Orai3 into liposomes for functional studies". Биохимия 88, nr 9 (15.12.2023): 1570–80. http://dx.doi.org/10.31857/s0320972523090099.
Pełny tekst źródłaFresquez, Adriana M., i 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, nr 1 (1.01.2022): C38—C48. http://dx.doi.org/10.1152/ajpcell.00490.2019.
Pełny tekst źródłaSmyth, Jeremy T., i James W. Putney. "Regulation of store-operated calcium entry during cell division". Biochemical Society Transactions 40, nr 1 (19.01.2012): 119–23. http://dx.doi.org/10.1042/bst20110612.
Pełny tekst źródłaGrimes, Derayvia, Ryan Johnson, Madeline Pashos, Celeste Cummings, Chen Kang, Georgia R. Sampedro, Eric Tycksen i in. "ORAI1 and ORAI2 modulate murine neutrophil calcium signaling, cellular activation, and host defense". Proceedings of the National Academy of Sciences 117, nr 39 (14.09.2020): 24403–14. http://dx.doi.org/10.1073/pnas.2008032117.
Pełny tekst źródłaTiffner, Adéla, i Isabella Derler. "Isoform-Specific Properties of Orai Homologues in Activation, Downstream Signaling, Physiology and Pathophysiology". International Journal of Molecular Sciences 22, nr 15 (27.07.2021): 8020. http://dx.doi.org/10.3390/ijms22158020.
Pełny tekst źródłaZhang, Xuexin, Ping Xin, Ryan E. Yoast, Scott M. Emrich, Martin T. Johnson, Trayambak Pathak, J. Cory Benson i in. "Distinct pharmacological profiles of ORAI1, ORAI2, and ORAI3 channels". Cell Calcium 91 (listopad 2020): 102281. http://dx.doi.org/10.1016/j.ceca.2020.102281.
Pełny tekst źródłaBaryshnikov, Sergey G., Maria V. Pulina, Alessandra Zulian, Cristina I. Linde i 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, nr 5 (listopad 2009): C1103—C1112. http://dx.doi.org/10.1152/ajpcell.00283.2009.
Pełny tekst źródłaLiu, Xiaoling, Tianyuan Zheng, Yan Jiang, Lei Wang, Yuchen Zhang, Qiyu Liang i Yuejie Chen. "Molecular Mechanism Analysis of STIM1 Thermal Sensation". Cells 12, nr 22 (12.11.2023): 2613. http://dx.doi.org/10.3390/cells12222613.
Pełny tekst źródłaRozprawy doktorskie na temat "Orai1"
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.
Pełny tekst źródłaJensen, 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.
Pełny tekst źródłaCalmodulin (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.
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.
Pełny tekst źródłaAlteration 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
Bartoli, Fiona. "Le canal calcique Orai1 : nouvel acteur impliqué dans la physiopathologie cardiaque". Thesis, Université Paris-Saclay (ComUE), 2018. http://www.theses.fr/2018SACLS027.
Pełny tekst źródłaWhile 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
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.
Pełny tekst źródłaClarysse, 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.
Pełny tekst źródłaWe 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
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.
Pełny tekst źródłaProstate 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
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/.
Pełny tekst źródłaDisturbance 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.
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/.
Pełny tekst źródłaGlycosylation with O-linked -N-acetyl-glucosamine (O-GlcNAc) is a highly dynamic post-translational modification. The process of O-GlcNAc is controlled by two enzymes: the OGT enzyme catalyses the addition of N-acetyl-glucosamine to the hydroxyl group of serine and threonine residues of a target protein, while OGA catalyzes the cleavage of O-GlcNAc from post-translationally-modified proteins. Proteins with an important role in vascular function are targets of O-GlcNAc and increased levels of proteins modified by O-GlcNAc increase vascular reactivity to contractile stimuli. The regulation of intracellular calcium (Ca2+) concentration, including the activation of STIM1/Orai1, is key in the control of vascular tone. The stromal interaction molecules (STIM) act as sensors of intracellular Ca2+ stores whereas the Orai proteins represent subunits of the Ca2+ release-activated Ca2+ channels (CRAC). We hypothesized that increased levels of vascular O-GlcNAc proteins augment vascular contractile responses by altering mechanisms that regulate the intracellular Ca2+. Rat thoracic aortas were incubated with PugNAc (OGA selective inhibitor, ) for 24h. Using an experimental protocol that evaluates contractions induced by Ca2+ influx and release, we demonstrated that incubation with PugNAc increases contractile responses to phenylephrine (PE) as well as the contraction induced by Ca2+ influx, after depletion of intracellular Ca2+ stores. The CRAC channel blockers, 2-APB (100 ) and gadolinium (Gd3+, 100 ), significantly reduced the contractions induced by Ca2+ influx in aortas incubated with PugNAc. Furthermore, these aortas showed increased STIM1 protein expression, which could result in increased influx of Ca2+ and, in turn, increase vascular contraction. The contraction induced by the release of intracellular Ca2+ stores, stimulated by caffeine (20 mM) and serotonin (10 ), was increased in aortas incubated with PugNAc. The Ca2+-ATPase (SERCA) inhibitor thapsigargin produced similar effects in arteries incubated with PugNAc or vehicle, despite the increased SERCA protein expression in aortas incubated with PugNAc. Since PKC is activated by increases in intracellular Ca2+ and arteries incubated with PugNAc show activation of PKC, we determined whether the activity of proteins that are targets of PKC was increased in PugNAc-treated aortas. Incubation with PugNAc increased the expression of phosphorylated forms of CPI-17, MYPT-1 and MLC. Together, these results suggest that activation of STIM1/Orai1, increased release of intracellular Ca2+ and PKC activation may represent mechanisms that modulate vascular responses upon increased O-GlcNAc proteins.
Cabanas, Hélène. "Rôle de la signalisation calcique dans la leucémie myéloïde chronique". Thesis, Poitiers, 2016. http://www.theses.fr/2016POIT2302/document.
Pełny tekst źródłaChronic Myeloid Leukemia (CML) is a clonal disease characterized by the presence of the Philadelphia chromosome encoding for Bcr-Abl, a constitutively active tyrosine kinase responsible for leukemogenesis. Although Bcr-Abl tyrosine kinase inhibitors (TKIs) have revolutionized the therapy of Ph+ leukemia, the complete eradication of CML is limited by the emergence of resistance in hematopoietic stem cells. This thesis proposes that calcium (Ca2+) signaling pathways, known to govern a large number of functions in normal and cancer cells, may be important in CML cell signaling. Therefore, we studied the role of Store Operated-Calcium entry (SOCE) (i.e. STromal Interaction Molecule 1 (STIM1), Orai1 and TRPC1 channels) and thrombin induced Ca2+ entry in leukemogenesis. We found a decrease in both calcium entries in Bcr-Abl-expressing cells compared to normal cells. The reduced SOCE seems related to a change in stoichiometry of Orai1/STIM1. This leads to a reduction of the Nuclear Factor of Activated T-cells (NFAT) translocation and functional consequences on cell proliferation and migration but not on apoptosis. Moreover, we showed that SOCE is restored in malignant cells after treatment with Imatinib, the main TKI. We proposed that Bcr-Abl expression could impact on Ca2+ homeostasis enhancing a general disorganization of cell functions in leukemia cells notably via Protein Kinase C (PKC) pathway. Altogether this work shows a deregulation of Ca2+ entry in Bcr-Abl-expressing cells, suggesting that the Ca2+ signaling pathway could be a therapeutic target in parallel with TKIs
Książki na temat "Orai1"
Arquivo Público do Distrito Federal (Distrito Federal, Brazil), red. Depoimentos orais: Catálogo. Wyd. 2. Brasília: Arquivo Público do Distrito Federal, 2008.
Znajdź pełny tekst źródłaArquivo Público do Distrito Federal (Distrito Federal, Brazil), red. Depoimentos orais: Catálogo. Wyd. 2. Brasília: Arquivo Público do Distrito Federal, 2008.
Znajdź pełny tekst źródłaKahakudo orai. Fukuoka-shi: Sogensha, 2004.
Znajdź pełny tekst źródła1930-, Preti Dino, Rodrigues Angela C. S i Projeto de Estudo da Norma Lingüística Urbana Culta de São Paulo., red. Análise de textos orais. São Paulo, SP: FFLCH/USP, 1993.
Znajdź pełny tekst źródłaArquivo Público do Distrito Federal (Distrito Federal, Brazil), red. Catálogo de depoimentos orais. Brasília: O Arquivo, 1994.
Znajdź pełny tekst źródłaS, Rodrigues Angela C., Preti Dino 1930- i Projeto de Estudo da Norma Lingüística Urbana Culta de São Paulo., red. Análise de textos orais. Wyd. 4. São Paulo, SP, Brasil: Humanitas Publicações, FFLCH/USP, 1999.
Znajdź pełny tekst źródłaRodrigues, Angela C. S., i Dino Preti. Análise de textos orais. Wyd. 7. São Paulo, SP, Brasil: Humanitas, 2010.
Znajdź pełny tekst źródła1930-, Preti Dino, Rodrigues Angela C. S i Projeto de Estudo da Norma Lingüística Urbana Culta de São Paulo., red. Análise de textos orais. São Paulo, SP: FFLCH/USP, 1993.
Znajdź pełny tekst źródłaOrain ghaoil: Amhráin ghrá. Baile Átha Cliath: Coiscéim, 1990.
Znajdź pełny tekst źródłaFred, Macaulay, red. Dòmhnall Ruadh Chorùna: Orain is dain. Loch nam Madadh, Uibhist a Tuath: Comann Eachdraidh Uibhist a Tuath, 1995.
Znajdź pełny tekst źródłaCzęści książek na temat "Orai1"
Yee, Christina. "Calcium Channel Defects (STIM1 and ORAI1)". W 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.
Pełny tekst źródłaYee, Christina. "Calcium Channel Defects (STIM1 and ORAI1)". W 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.
Pełny tekst źródłaDerler, Isabella, Josef Madl, Gerhard Schütz i Christoph Romanin. "Structure, Regulation and Biophysics of ICRAC, STIM/Orai1". W Advances in Experimental Medicine and Biology, 383–410. Dordrecht: Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-94-007-2888-2_16.
Pełny tekst źródłaWoo, Jin Seok, Sonal Srikanth i Yousang Gwack. "Modulation of Orai1 and STIM1 by Cellular Factors". W 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.
Pełny tekst źródłaCheng, Kwong Tai, Hwei Ling Ong, Xibao Liu i Indu S. Ambudkar. "Contribution of TRPC1 and Orai1 to Ca2+ Entry Activated by Store Depletion". W Transient Receptor Potential Channels, 435–49. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-94-007-0265-3_24.
Pełny tekst źródłaZhou, Yandong, Youjun Wang i Donald L. Gill. "Assessing the Molecular Nature of the STIM1/Orai1 Coupling Interface Using FRET Approaches". W 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.
Pełny tekst źródłaCioffi, Donna L., Christina Barry i Troy Stevens. "Store-Operated Calcium Entry Channels in Pulmonary Endothelium: The Emerging Story of TRPCS and Orai1". W 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.
Pełny tekst źródłaPacheco, Jonathan, A. Bohórquez-Hernández, Kevin M. Méndez-Acevedo, Alicia Sampieri i Luis Vaca. "Roles of Cholesterol and PtdIns(4,5)P2 in the Regulation of STIM1–Orai1 Channel Function". W Advances in Experimental Medicine and Biology, 305–26. Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-21547-6_11.
Pełny tekst źródłaSalido, Gines M., Isaac Jardín i Juan A. Rosado. "The TRPC Ion Channels: Association with Orai1 and STIM1 Proteins and Participation in Capacitative and Non-capacitative Calcium Entry". W Transient Receptor Potential Channels, 413–33. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-94-007-0265-3_23.
Pełny tekst źródłaBartoli, Fiona, i Jessica Sabourin. "Cardiac Remodeling and Disease: Current Understanding of STIM1/Orai1-Mediated Store-Operated Ca2+ Entry in Cardiac Function and Pathology". W Store-Operated Ca²⁺ Entry (SOCE) Pathways, 523–34. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-57732-6_26.
Pełny tekst źródłaStreszczenia konferencji na temat "Orai1"
Hubrack, Satanay, Ethel Adap, Stefan Feske i Khaled Machaca. "Role Of Stim1 And Orai1 In Mammalian Oocyte Activation". W Qatar Foundation Annual Research Conference Proceedings. Hamad bin Khalifa University Press (HBKU Press), 2014. http://dx.doi.org/10.5339/qfarc.2014.hbpp0176.
Pełny tekst źródłaHubrack, Satanay Zuhair, Awab Ibrahim i Khaled Machaca. "Study of the Effect of Calreticulin on Orai1 Function". W Qatar Foundation Annual Research Conference Proceedings. Hamad bin Khalifa University Press (HBKU Press), 2016. http://dx.doi.org/10.5339/qfarc.2016.hbpp1846.
Pełny tekst źródłaAhmad, S., J. Wrennall, M. Sassano i R. Tarran. "ELD607, a Novel Anti-Orai1 Peptide Reduces Pulmonary Inflammation". W 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.
Pełny tekst źródłaMasson, Bastien, Hélène Le Ribeuz, Jessica Sabourin, Emily Woodhouse, Richard Foster, Yann Ruchon, Mary Dutheil i in. "Late Breaking Abstract - Involvement of Orai1 Ca2+ channel in the pathogenesis of pulmonary arterial hypertension. Orai1 as a new potential therapeutic target ?" W ERS International Congress 2021 abstracts. European Respiratory Society, 2021. http://dx.doi.org/10.1183/13993003.congress-2021.pa599.
Pełny tekst źródłaPelzl, L., I. Sahu, D. Heinzmann, A. A. M. Bhuyan, T. a. Maghout, I. Marini, F. Rigoni i in. "Phosphate-induced ORAI1 Expression and Store Operated Ca2+ Entry in Megakaryocytes". W 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.
Pełny tekst źródłaLatour, Simon, Isabelle Mahouche, Floriane Cherrier, Jean-Philippe Merlio, Sandrine Poglio i Laurence Bresson Bepoldin. "Abstract 1881: STIM1 and Orai1 control non-Hodgkin lymphoma cells migration". W 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.
Pełny tekst źródłaAhmad, S., M. Biggart, F. Sassano, A. Ghosh i R. Tarran. "The Orai1 Antagonist, ELD607, Reduces Chronic Neutrophilic Inflammation in βENaC Mice". W 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.
Pełny tekst źródłaDib, Maya, Rawad Hodeify i Khaled Machaca. "Identification Of Proteins Involved In Orai1 Trafficking By Mass Spectrometry-based Approach". W Qatar Foundation Annual Research Conference Proceedings. Hamad bin Khalifa University Press (HBKU Press), 2014. http://dx.doi.org/10.5339/qfarc.2014.hbpp048.
Pełny tekst źródłaTarran, R., S. Ahmad, J. Wrennal, E. N. Worthington i M. F. Sassano. "Local Orai1 Inhibition Reduces Pulmonary Inflammation in House Dust Mite-Exposed Mice". W 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.
Pełny tekst źródłaYang, Shengyu, Jianwei Sun i Huifang He. "Abstract 4317: Stim1 and Orai1 are critical regulators of melanoma invasion and anoikis". W 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.
Pełny tekst źródłaRaporty organizacyjne na temat "Orai1"
Huang, Xin-Yun. Orai1 as New Therapeutic Target for Inhibiting Breast Tumor Metastasis. Fort Belvoir, VA: Defense Technical Information Center, wrzesień 2009. http://dx.doi.org/10.21236/ada518249.
Pełny tekst źródłaCanto, Patricia, red. Euskal Autonomia Erkidegoko Lehiakortasunari buruzko 2021eko Txostena. Ongizatea helburu duen lehiakortasuna eraikitzea. Universidad de Deusto, 2021. http://dx.doi.org/10.18543/zemz8571.
Pełny tekst źródłaSchmidt-Sane, Megan, i 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, maj 2023. http://dx.doi.org/10.19088/sshap.2023.009.
Pełny tekst źródłaNazioen 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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