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Добірка наукової літератури з теми "ORAOV1"

Автор: Grafiati

Опубліковано: 10 березня 2023

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Статті в журналах з теми "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.

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Oral cancer overexpressed 1 ( ORAOV1) is a crucial oncogene in oral squamous cell carcinoma (OSCC). In this study, we have identified a novel splice variant of ORAOV1, designated as ORAOV1-A. To study the potential role of ORAOV1-A in OSCC, we tested its expression in 7 OSCC cell lines, as well as in 19 normal oral tissue samples and 47 OSCC tissue samples. The expression of ORAOV1-A was detectable in 6 out of 7 OSCC cell lines tested. In OSCC tissue samples, the expression frequency of ORAOV1-A (51.1%) was much higher than that in normal samples (10.5%). Notably, an inverse correlation was found between the expression frequency of ORAOV1-A and the degree of differentiation in OSCC ( P = 0.0017). In conclusion, our results suggested that ORAOV1-A may play a functional role in the tumorigenesis of OSCC, and ORAOV1-A expression may serve as an adjunctive prognostic indicator for persons with OSCC.

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Xavier, 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.

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Салеева, 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.

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Цель. Определение прогностической значимости и роли экспрессии некодирующих РНК (длинные РНК и микроРНК), и белка кодирующих генов в патогенезе рака гортани. Методика. Исследован биопсийный материал и периферическая кровь 35 пациентов с диагнозом плоскоклеточный рак гортани (ПРГ) с классификацией от T1N0M0 до T4N1M0. Контролем служили образцы близлежащей гистологически неизмененной ткани гортани тех же больных. Для оценки экспрессии генов исследовали кровь 27 здоровых доноров. Содержание мРНК генов ( р53, CCND1, ORAOV1, hPTEN ), длинных некодирующих РНК (днРНК): NEAT1, MALAT1, ROR , а также зрелых микроРНК (miR-21, miR-27a, miR-34a, miR-101, miR-124, miR-125b, miR-181а) в опухолевой ткани и крови определяли методом ПЦР в реальном времени (ПЦР-РВ). Результаты. Выявлено увеличение содержания мРНК генов CCND1, hPTEN , днРНК NEAT1, MALAT1 и miR-21, miR-27a в крови у пациентов с ПРГ. Установлено, что уровень мРНК генов CCND1, ORAOV1 был значимо выше при исследовании биоптатов у больных 3-й - 4-й стадии, чем у больных 1-й - 2-й стадии заболевания. Такая же закономерность выявлена для днРНК NEAT1, MALAT1 и для miR-101. Экспрессия miR-27a и miR-124 на более поздних стадиях болезни была ниже, чем у пациентов 1-2 стадии. Заключение. Выявлена возможность использования исследованных днРНК, микроРНК и мРНК белоккодирующих генов для индивидуального прогноза заболевания при создании панели биомаркеров. Aim. To study the role of non-coding RNA (long RNAs and microRNAs) expression and protein-coding genes in the pathogenesis of laryngeal cancer to determine their prognostic significance for oncotransformation. Methods. The expression of long non-coding RNAs, microRNAs and protein-coding genes was examined in biopsy samples (fresh frozen tissue) and peripheral blood samples from 35 patients with laryngeal squamous cell cancer (LSCC) at T1N0M0 - T4N1M0 stages. Samples of surrounding, histologically unchanged tissues collected from the same patients were used as control. Gene expression was evaluated in blood samples from 27 healthy donors. Contents of gene mRNAs ( p53, CCND1, ORAOV1, hPTEN ), long non-coding RNAs (IncRNA) ( NEAT1, MALAT1, ROR ), and mature miRNAs (miR-21, miR-27a, miR-34a, miR-101, miR-124, miR -125b, miR-181a) were measured in tissue and blood using real-time PCR. Results. Contents of CCND1 and hPTEN gene mRNAs, lncRNAs ( NEAT1, MALAT1), miR-21, and miR-27a were increased in blood of patients with LSCC. Levels of CCND1 and ORAOV1 gene mRNAs were significantly higher in biopsy samples from stage 3-4 patients compared to stage 1-2 patients. A similar expression pattern was observed for lncRNAs NEAT1 and MALAT1 and miR-101. On the other hand, expression of miR-27a and miR-124 was lower at later stages than at stages 1-2. Conclusion. The studied lncRNAs, microRNAs and protein-coding genes can be used in development of a biomarker panel for individual prognosis of the disease.

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Jiang, 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.

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Togashi, 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.

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Prusty, 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.

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Salmon 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.

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Zhao, 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.

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Jiang, 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.

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Togashi, 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.

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Більше джерел

Дисертації з теми "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.

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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 Orai1 in Bezug auf die Aktivierung und Entwicklung von Lymphozyten sowie auf die pathogenetische Bedeutung für humane Immundefektsyndrome zum Ziel. So konnte hier durch das Sequenzieren genomischer DNA mehrerer SCID-Patienten eine neue Mutation in Orai1 aufgedeckt werden. Mithilfe intrazellulärer Durchflusszytometrie und Real-Time-PCR gelang es, die Expression von Orai1 auf humanen und murinen Immunzellen, einschließlich T- und B-Lymphozyten, nachzuweisen. Darüber hinaus wurden Orai1 „knock-in“ Mäuse analysiert, welche transgen für eine bei zwei SCID-Patienten gefundene Mutation (R91W) (Feske, S. et al. 2006) sind. Dadurch war es möglich die Funktion von Orai1 und die des CRAC-Kanal vermittelten Ca2+-Einstroms für die Entwicklung und Aktivierung von Lymphozyten zu analysieren. Diese transgenen Mäuse stellen das zu diesem Zeitpunkt erste Tiermodell dar, mit dessen Hilfe die Rolle von CRAC-Kanälen in vivo studiert werden kann.

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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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Calmodulin (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 (K_a = 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.

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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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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)/NFAT (Nuclear factor of activated T-cells). Au contraire, une inhibition fonctionnelle ou une extinction génique des canaux TRPCs et de la protéine STIM1 serait cardioprotectrice contre le stress hypertrophique. Cependant, le rôle physiopathologique des canaux calciques Orai1 dans le cœur reste, à ce jour, méconnu et débattu puisque son extinction in vitro présente un effet bénéfique contre l’hypertrophie des cardiomyocytes alors que son extinction in vivo présente des effets délétères avec le développement d’une cardiomyopathie dilatée. De plus amples investigations quant au rôle d’Orai1 dans la physiopathologie cardiaque apparaissent donc primordiales. De ce fait, les objectifs de ma thèse sont d’explorer le rôle de la signalisation calcique dépendante d’Orai1 dans le cœur dans des conditions physiologiques et pathologiques grâce à un modèle de souris transgéniques exprimant un mutant non fonctionnel d’Orai1, spécifiquement dans le cœur (dn-Orai1R91W/tTa) et un inhibiteur pharmacologique sélectif, le JPIII. Tout d’abord, nous montrons que les souris dn-Orai1R91W/tTa présentent une fonction cardiaque normale et une homéostasie calcique impliquée dans le couplage excitation-contraction conservée suggérant qu’Orai1 n’a pas de rôle majeur dans le coeur adulte en condition physiologique. Cependant, nous avons démontré une augmentation de l’expression et de l’activité d’Orai1 dans un modèle murin d’hypertrophie cardiaque induite par surcharge de pression, qui serait délétère pour la fonction ventriculaire. Au contraire, l’inhibition fonctionnelle d’Orai1 par manipulation génétique ou par l’outil pharmacologique (JPIII) semble protéger le coeur des dysfonctions ventriculaires au cours de l’hypertrophie. Cet effet bénéfique passerait par une restauration de l’homéostasie calcique et notamment par un maintien de l’expression de la pompe ATPase SERCA2a. Nous avons également mis en évidence que la voie de l’aldostérone/récepteurs aux minéralocorticoïdes modulait l’expression des canaux TRPC1, -C4, -C5 et notamment Orai1 via la protéine SGK1 (Serum and Glucocorticoid-regulated Kinase 1) dans les cardiomyocytes ventriculaires de rat nouveaux-nés. L’activation de cette voie de signalisation pourrait être à l’origine de la surexpression des canaux TRPCs/Orai1 retrouvée au cours de l’hypertrophie cardiaque. Ces travaux décrivent donc Orai1 comme une cible thérapeutique potentielle dans le traitement de l’hypertrophie cardiaque et de l’IC
While 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

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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 affecter les cellules mammaires normales. L'objectif de ma thèse est d'étudier les mécanismes moléculaires par lesquels CO-OCS induit ses effets anti-tumoraux. CO-OCS inhibe la migration des cellules cancéreuses à fort potentiel métastatique. Cet effet anti-migratoire est dû à une réduction de l'expression de la β1-intégrine, de Stim1, et de l'activation des voies de signalisation FAK et ERK1/2 par CO-OCS. Dans les cellules cancéreuses peu invasives, CO-OCS diminue la prolifération et augmente la mortalité de ces cellules en affectant l'expression de 3 protéines : Stim1 et Orai1 : protéines N-glycosylées au niveau du réticulum endoplasmique (RE), et GRP78, protéine de stress du RE. Ainsi en supprimant complétement l'expression de Stim1, CO-OCS réduit la prolifération en accumulant les cellules dans les phases G1 et G2/M du cycle cellulaire. Alors que la réduction de l'expression de GRP78 et d'Orai1 par le CO-OCS augmente respectivement l'apoptose et la nécrose. Par ailleurs, l'invalidation de Stim1 atténue l'effet apoptotique induit par CO-OCS. CO-OCS réduit aussi le contenu calcique du RE. Cette réduction du calcium réticulaire est due à une fuite de calcium par le Translocon. En effet, l'Anisomycine, inhibiteur du Translocon, restore de contenu calcique réticulaire et antagonise l'apoptose induite par le CO-OCS. En conclusion, CO-OCS induit une accumulation de protéines mal-repliées dans le RE induisant ainsi un stress réticulaire. Trois cibles du CO-OCS ont été identifiées : l'expression de Stim1 favorise la prolifération tandis que celle d'Orai1 et de GRP78 protègent respectivement les cellules de l'apoptose et de la nécrose induites par CO-OCS. De plus, en diminuant l'expression de GRP78, CO-OCS induit une fuite du calcium du RE par le Translocon
Alteration 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

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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 dans le CaP a déjà été montrée dans de précédentes études, via leur implication dans les canaux de type SOC (store-operated calcium channel) et ARC (arachidonic acid-regulated channel). Cependant, le rôle du canal Orai1 dans la prolifération du CaP, ou son éventuelle implication dans la physiologie des CSC, restaient inconnus. Parallèlement, pour répondre aux limitations de son ciblage direct, nous avons cherché à identifier ses protéines partenaires. Nous nous sommes ainsi intéressés au récepteur Sigma 1 (S1R), une protéine chaperonne dont l’expression augmente dans le CaP, et qui possède de nombreux modulateurs pharmacologiques utilisés en clinique. Ce travail avait donc un double objectif : étudier le rôle d’Orai1 dans le CaP et les CSC prostatiques, et caractériser fonctionnellement le rôle du S1R en tant que nouveau partenaire du canal Orai1. Ces travaux ont tout d’abord permis de mettre en évidence l’importance d’Orai1 dans le contrôle de la transition entre la quiescence et la prolifération des CSCs prostatiques via la voie NFAT. De plus, ces résultats ont été confirmés dans les CSCs de mélanome, montrant que le rôle d’Orai1 serait généralisable au-delà du modèle prostatique. Nous avons également montré que le S1R interagit directement avec Orai1 et module positivement son activité, impactant ainsi la prolifération des cellules cancéreuses prostatiques. Enfin, nous avons mis en évidence la régulation de l’expression de ces protéines par les androgènes, ce qui est d’importance cruciale dans l’évolution du CaP. Nos résultats ont donc permis l’identification d’un acteur central du contrôle de la prolifération du CaP (Orai1), et la caractérisation d’une nouvelle protéine partenaire du canal Orai1 dans le CaP : le S1R. Ces travaux montrent que le S1R et Orai1 pourraient constituer de nouveaux marqueurs intéressants, ainsi que de potentielles nouvelles cibles thérapeutiques
Prostate 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

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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 ainsi son inhibition de la transcription du gène KCNN3 (codant pour SK3) ; ii) favorise la migration cellulaire dépendante du canal SK3, mécanisme impliquant également le CaSR ; iii) active le canal SK3 qui, par ailleurs, voit son activité réduite par l’élévation d’AMPc intracellulaire. De plus, l’augmentation d’AMPc délocalise un canal calcique partenaire de SK3, le canal Orai1, et diminue l’entrée constitutive de Ca²+ et la migration dépendantes du canal SK3. En conclusion, nos résultats montrent que l’expression et l’activité de SK3 sont régulées par l’AMPc et le Ca2+ extracellulaire. Ceci permet d’envisager une nouvelle stratégie thérapeutique ciblant l’AMPc pour le traitement des métastases osseuses du cancer du sein
We 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

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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.

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Thesis (M.S.)--Massachusetts Institute of Technology, Dept. of Architecture, 1995.
Includes 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.

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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.

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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/Orai1 pode representar um novo mecanismo que modula alterações vasculares nos níveis de Ca2+ intracelular na hipertensão arterial e que contribui para as diferenças sexuais de reatividade vascular em animais hipertensos.
Disturbance 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.

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Книги з теми "ORAOV1"

Orahova ljuska. Beograd: Čigoja štampa, 2003.

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Bochow, Karl-Heinz. Orava. Leipzig: Brockhaus, 1990.

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Sijarić, Ćamil. Miris lišća orahova. Sarajevo: Preporod, 2004.

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Peter, Huba, and Mikláš Milan, eds. Premeny Oravy. Martin: Vyd. Osveta, 1985.

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author, 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.

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Benović, Ljubica. Kliješta za razbijanje orahove ljuske. Grude: Ogranak matice hrvatske Grude, 2006.

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Kliješta za razbijanje orahove ljuske. Grude: Ogranak matice hrvatske Grude, 2006.

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Matovcik, Augustin. Hviezdoslav a rodna Orava. Martin: Matica slovenska, 1999.

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Langer, Juraj. Cesty po minulosti Oravy. [Slovakia]: Peter Huba, 1993.

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Orav, Maie. Maie Orava tantsud II. Rakvere: Tarvanpää Selts, 2003.

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Частини книг з теми "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.

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Ghosh, 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.

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Yee, 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.

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Yee, 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.

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Bandia, 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.

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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, 383–410. Dordrecht: 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, 73–92. Boca Raton : Taylor & Francis, 2017. | Series: Methods in signal transduction series: 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, 435–49. Dordrecht: 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, 127–44. Boca Raton : Taylor & Francis, 2017. | Series: Methods in signal transduction series: 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, 137–54. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60761-500-2_9.

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Тези доповідей конференцій з теми "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.

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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, 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.

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Pelzl, 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.

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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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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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Hodeify, 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.

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Звіти організацій з теми "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.

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