Tesis sobre el tema "Store Operated Calcium Channels"
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Zeng, Bo. "Pharmacological regulation and function of store-operated calcium channels". Thesis, University of Hull, 2012. http://hydra.hull.ac.uk/resources/hull:6432.
Texto completoBonds, Timetria. "Store-Operated Calcium Channels in the Function of Intracardiac Neurons". Scholar Commons, 2012. http://scholarcommons.usf.edu/etd/3983.
Texto completoCovington, Elizabeth D. "Oligomerization and dynamic clustering underlying activity of store-operated calcium channels /". May be available electronically:, 2009. http://proquest.umi.com/login?COPT=REJTPTU1MTUmSU5UPTAmVkVSPTI=&clientId=12498.
Texto completoArunachalam, Sasi. "The Role of store operated calcium channels in human carcinoid cell lines". University of Toledo Health Science Campus / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=mco1279216983.
Texto completoDouglas, Sophie Georgina. "Regulation of CRAC channels and agonist-induced Ca2+ signals". Thesis, University of Oxford, 2012. http://ora.ox.ac.uk/objects/uuid:ae94ca14-ac95-4ea6-b14a-14f9f7bafd63.
Texto completoLuik, Riina M. "Molecular mechanisms of store-operated calcium signaling : local activation of CRAC channels by STIM1, the ER calcium sensor /". May be available electronically:, 2007. http://proquest.umi.com/login?COPT=REJTPTU1MTUmSU5UPTAmVkVSPTI=&clientId=12498.
Texto completoBose, Diptiman Dipen. "Study of pharmacological and physiological factors regulating store operated calcium channels in a neuronal cell line". Scholarly Commons, 2006. https://scholarlycommons.pacific.edu/uop_etds/2650.
Texto completoJones, Lynette. "The role of IP3 receptors 1 and 2 in the activation of store-operated calcium channels in rat liver cells /". Title page and abstract only, 2005. http://web4.library.adelaide.edu.au/theses/09SB/09sbj762.pdf.
Texto completoMcElroy, Stuart Patrick. "Store operated calcium entry and TRPC channel expression in rat pulmonary artery smooth muscle cells". Thesis, University of Strathclyde, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.426332.
Texto completoCastro, Kraftchenko Joel y kraf0005@flinders edu au. "STORE OPERATED Ca2+ CHANNELS IN LIVER CELLS: REGULATION BY BILE ACIDS AND A SUB-REGION OF THE ENDOPLASMIC RETICULUM". Flinders University. Medicine, 2008. http://catalogue.flinders.edu.au./local/adt/public/adt-SFU20080826.135311.
Texto completoBonnefond, Marie-Laure. "Rôle de la signalisation calcique dans la sensibilisation des cancers ovariens chimiorésistants aux stratégies anti-Bcl-xL". Thesis, Normandie, 2017. http://www.theses.fr/2017NORMC424.
Texto completoOvarian cancer is the leading cause of death from gynecological cancer. There is an urgent need to find new therapeutic strategies due to failure of treatments associated to development of chemoresistance. In this context, the laboratory has shown the cooperation of two anti-apoptotic proteins overexpressed in ovarian cancer, Mcl-1 and Bcl-xL, for preventing apoptotic cell death. ABT-737, a Bcl-xL inhibitor BH3-mimetic, was developed by Abbvie and has a clinically derivative named ABT-263. In contrast, no Mcl-1 inhibitor is currently available in clinic. The inhibition of this anti-apoptotic protein is therefore one of the objectives of the laboratory. Since inhibition of PI3K / Akt / mTOR signaling pathway leads to inhibition of Mcl-1 expression and calcium is able to modulate this pathway, we wondered if the modulation of calcium fluxes allowed the inhibition of Mcl-1 in ovarian cancer cells. First we were able to show that calcium chelation by BAPTA-AM allowed to inhibit Mcl-1 expression via mTORC1 pathway and to sensitize the cells to ABT-737. In a second step, we investigated the effect of an inhibitor of calcium fluxes that is evaluated in clinical studies, carboxyamidotriazole. We show that the inhibition of capacitive calcium channels could lead to Mcl-1 down-expression via inhibition of mTORC1 and promote apoptosis in combination with ABT-737. Finally, we observed that CAI induces a morphological change resulting in cell death. This type of death seems to be related to disruption of metabolism in IGROV1-R10 cancer cells and would be close to a cell death recently described in the literature: autosis
Terrie, Élodie. "Rôle de la signalisation calcique dépendante des Store-Operated Channels (SOC) dans les cellules souches neurales adultes et les cellules souches cancéreuses de glioblastomes". Thesis, Poitiers, 2019. http://www.theses.fr/2019POIT2322.
Texto completoNeural stem cells (NSC) persist in the brain of adult mammals and fuel the brain with new neurons and glial cells all lifelong. Recruited by brain injuries, NSC are considered with great interest by regenerative medicine. However, the development of new therapeutic approaches based on the use of NSC requires an in-depth knowledge of the mechanism regulating these cells. Glioblastomas are the most frequent and deadliest form of adult brain tumors. Within the tumor, glioblastoma stem cells (GSC) form a subpopulation of cells that is considered as responsible of tumor initiation, propagation and relapse, as these cells are particularly resistant to anti-tumoral treatments. GSC and NSC share key characteristics and numerous studies suggest that GSC arise from transformed NSC. Transcriptomic analysis of NSC and of GSC revealed an enrichment of calcium signaling transcripts in these two cell populations. Representing a major way of calcium influx into cells, Store-Operated Channels (SOC) are mobilized in response to a wide range of extracellular factors. SOC regulate many cellular processes and are often hijacked in cancer to promote tumor progression.The aim of this thesis is to evaluate potential SOC involvement in NSC and GSC regulation.The first part of this work, relying on in vitro and in vivo studies, demonstrates that NSC from adult mice express functional SOC whose inhibition by pharmacological agents reduces NSC proliferation and self-renewal. In the second part of this thesis, we demonstrate that GSC from primary cultures derived from patients express SOC, as do NSC, and that SOC inhibition reduces GSC ability to proliferate and self-renew.Accordingly, the results of this thesis demonstrate that SOC regulate NSC and GSC self-renewal, a property that is essential to maintain stem cells pool. As GSC are responsible for glioblastomas treatment resistance, our studies point to a potential new therapeutic way, via calcium channels, against this deadly pathology
Batchelor, Helen R. "Characterisation of store-operated calcium entry in a vascular endothelial cell line and impact on the production of nitric oxide". Thesis, University of Oxford, 2014. https://ora.ox.ac.uk/objects/uuid:548a6062-2b2f-46ce-b91a-890561b5edff.
Texto completoVanden, Abeele Fabien. "Caractérisation moléculaire et fonctionnelle des canaux calciques de type SOC (Store Operated Channel) : implication dans la cancerogénese prostatique". Lille 1, 2003. https://pepite-depot.univ-lille.fr/RESTREINT/Th_Num/2003/50376-2003-221.pdf.
Texto completoVieira, Elaine. "Signal Transduction of Glucagon Secretion". Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-6319.
Texto completoKawasaki, Brian Takeshi. "Players in the regulation of calcium entry activation of the transient receptor potential channels by src tyrosine kinase and a distinct role for the IP3 receptor c-terminus in store- and receptor-operated calcium entry /". Diss., Restricted to subscribing institutions, 2005. http://proquest.umi.com/pqdweb?did=994232031&sid=9&Fmt=2&clientId=1564&RQT=309&VName=PQD.
Texto completoFlorent, Romane. "Intérêt de la modulation pharmacologique des voies de signalisation calcique pour restaurer le contrôle de l'apoptose dans les cancers ovariens chimiorésistants Inhibition of store-operated channels by carboxyamidotriazole sensitizes ovarian carcinoma cells to anti-BclxL strategies through Mcl-1 down-regulation Drug Repositioning of the α1-Adrenergic Receptor Antagonist Naftopidil: A Potential New Anti-Cancer Drug? Bim, Puma and Noxa upregulation by Naftopidil sensitizes ovarian cancer to the BH3-mimetic ABT-737 and the MEK inhibitor Trametinib". Thesis, Normandie, 2020. http://www.theses.fr/2020NORMC413.
Texto completoThe poor prognosis of ovarian cancer is mainly explained by a high rate of resistance to conventional chemotherapy presented by patients. Therefore, discovery of both alternative therapeutic strategies to chemotherapy and predictive biomarkers for response to this treatment represent a major challenge for improving the management of this pathology. Chemoresistance of ovarian cancer cells is mainly due to their resistance to apoptosis, resulting from an imbalance between the pro- and anti-apoptotic members of the Bcl-2 family that control this type of cell death. Thus, all strategies able to modulate the [pro]/[anti-apoptotic] protein ratio in favor of [pro-] effectively restore apoptosis in these cells. However, calcium signaling is known to regulate the expression of these proteins and thus appears to be a relevant target for restoring apoptosis in chemoresistant ovarian cancer cells. In this context, we have shown that three calcium signal modulators are able to induce the death of these cells in association with ABT-737, a BH3-mimetic targeting the activity of the anti-apoptotic Bcl-xL. This sensitization to ABT-737 is enabled by the fact that carboxyamidotriazole represses the expression of the anti apoptotic Mcl-1 via the inhibition of SOCE currents, naftopidil increases pro-apoptotic protein expression via ER stress induction or JNK activation and thapsigargin seems to prepare cell death through increasing intracellular calcium concentration via STIM1 and, maybe, through Noxa expression induction. In addition, players of the calcium signaling toolkit, known to undergo remodeling during carcinogenesis could be proven as tools for predicting response to chemotherapy. In this context, we have shown that the expression of the calcium pump SERCA2 seems to play a role as a predictive biomarker for response to chemotherapy of patients with ovarian cancer
Zhang, Changfeng. "Investigation of the endoplsmic reticulum calcium stores for their potential roles in neuroprotection using the NG115-401L neuronal cell line model". Scholarly Commons, 2014. https://scholarlycommons.pacific.edu/uop_etds/142.
Texto completoNg, Lih Chyuan. "Store-operated channels in rat pulmonary artery". Thesis, University of Strathclyde, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.248256.
Texto completoNash, Katherine Louise. "Store-operated calcium entry in human spermatozoa". Thesis, University of Birmingham, 2012. http://etheses.bham.ac.uk//id/eprint/3260/.
Texto completoDi, Capite Joseph Lister. "Store-operated calcium entry and mast cell function". Thesis, University of Oxford, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.509920.
Texto completoBailey, Marc Aaron. "Store operated calcium entry in abdominal aortic aneurysm". Thesis, University of Leeds, 2016. http://etheses.whiterose.ac.uk/13678/.
Texto completoDjillani, Alaeddine. "Caractérisation des canaux calciques dans les polynucléaires neutrophiles : rôle dans la phagocytose et la production des radicaux libres oxygénés". Phd thesis, Université Paris Sud - Paris XI, 2013. http://tel.archives-ouvertes.fr/tel-01069097.
Texto completoHao, Baixia y 郝佰侠. "Regulatory and functional studies of store-operated calcium entry". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hdl.handle.net/10722/196486.
Texto completopublished_or_final_version
Physiology
Doctoral
Doctor of Philosophy
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.
Texto completoHarper, A. G. S. "The mechanisms underlying the activation of store-operated calcium entry in human platelets". Thesis, University of Cambridge, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.603727.
Texto completoWhitworth, Claire Leanne. "Phenotype-specific store-operated calcium entry and the differentiation response in neuroblastoma cells". Thesis, University of Newcastle upon Tyne, 2016. http://hdl.handle.net/10443/3404.
Texto completoMcIvor, Emma. "Modelling store operated calcium entry : creating a three dimensional spatio-temporal model to predict local calcium signals". Thesis, University of Nottingham, 2018. http://eprints.nottingham.ac.uk/55110/.
Texto completoSharmeen, Cynthia. "Involvement of Beta-arrestin 1 and Beta-arrestin 2 in store operated calcium entry". Mémoire, Université de Sherbrooke, 2016. http://hdl.handle.net/11143/9499.
Texto completoAbstract : In an organism, intracellular [Ca2+] takes part in many biological processes. Eukaryotic cells express a variety of channels in the plasma membrane through which calcium can enter. In non-excitable cells, two main mechanisms allow calcium entry; the store-operated calcium entry via Orai1 (SOCE) and receptor-operated calcium entry (ROCE). Several key proteins are involved in the regulation of these calcium entry pathways as well as in calcium homeostasis. TRPC6 is a calcium channel implied in calcium entrance into the cells following hormonal stimulation and translocates to the plasma membrane. TRPC6 channel appear to the plasma membrane until the stimulus is present. Although, the mechanisms that regulate the trafficking and activation of TRPC6 are still little known. Recent findings have demonstrated that there is a potential role of Rho kinase in activity of TRPC6. Rho kinase is activated by the small G protein RhoA that itself can be activated by the heterotrimeric G proteins Gα12 and Gα13. In addition to Gα12 and Gα13 proteins, cytosolic GPCR desensitizing proteins β-arrestin 1 and/or β-arrestin 2 could also activate RhoA. The purpose of our study is to investigate the involvement of the proteins Gα12/13 and β-arrestin 1/β-arrestin 2 in the activation of TRPC6 and Orai1 protein. We used siRNA specific to Gα12/13 or β-arrestin 1/β-arrestin 2 to knockdown their endogenous expression. Then, calcium imaging in real time was performed in order to see the quantity of calcium entered into the cell following stimulation by vasopressin (AVP), thapsigargin, or carbachol. We hence identified that in A7r5 cell, vascular smooth muscle cell where TRPC6 channel expressed endogenously; reduced expression of Gα12 or Gα13 proteins does not seem to modify the AVP-induced Ca2+ entry compared to control cells. On the other hand, calcium imaging experiment in knocked down β-arrestin 1 or β-arrestin 2 in HEK 293 cells as well as HEK 293 cells stably transfected with TRPC6 (T6.11 cells) resulted in an increased thapsigargin-induced calcium entry. The co-immunoprecipitation studies demonstrate an interaction between β-arrestin 1 and STIM1, a calcium sensor in SOCE influx, while no interaction was observed between β-arrestin 1 and Orai1.We moreover showed by confocal microscopy that reduced expression of β-arrestin 1/ β-arrestin 2 does not influence the quantity of Orai1 at the cell periphery. Preliminary results showed that reduced expression of β-arrestin 1 or β-arrestin 2 increases the quantity of STIM1-YFP in the intracellular space and less it’s in peri-membrane space. In conclusion, we showed that β-arrestin 1 or β-arrestin 2 are involved in the store-operated calcium entry (SOCE) and control the quantity of STIM1 in the endoplasmic reticulum.
Wallace, Patrick. "Excitation/contraction coupling in mouse anococcygeus smooth muscle : a role for store-operated calcium entry". Thesis, King's College London (University of London), 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.424303.
Texto completoNassrallah, Wissam. "Store-Operated Response in CA1 Pyramidal Neurons Exhibits Features of Homeostatic Synaptic Plasticity". Thesis, Université d'Ottawa / University of Ottawa, 2015. http://hdl.handle.net/10393/33357.
Texto completoBlackman, Sarah Kathryn. "Contribution of Calcium Entry through Non-Voltage Operated Calcium Channels to the Contractile Response of Vascular Smooth Muscle to Agonists". Thesis, King's College London (University of London), 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.487202.
Texto completoEndo, Yukari. "Dominant mutations in ORAI1 cause tubular aggregate myopathy with hypocalcemia via constitutive activation of store-operated Ca2+ channels". Kyoto University, 2015. http://hdl.handle.net/2433/198937.
Texto completoBoutry, Maxime. "Dysfonctions des lysosomes et neurodégénérescence : l'exemple de la paraplégie spastique de type SPG11". Thesis, Paris 6, 2017. http://www.theses.fr/2017PA066295/document.
Texto completoLysosomal dysfunctions are involved in a large number of neurodegenerative diseases highlightingthe crucial function of lysosomes in neuron survival and function. The mechanism of lysosomereformation from autolysosomes allow cells to maintain the ool of functional lysosomes.Disruptions of this rocess are involved in athologies affecting the central nervous system. Inparticular, spatacsin that lays a role in lysosome recycling is implicated in hereditary spasticparaplegia type SPG11, a severe disease characterized by motors and cognitive alterations. Thispathology is caused by loss of function mutations in SPG11, encoding spatacsin. The study ofSPG11 cellular models gives the opportunity to decipher the hysiopathological mechanismsunderlying lysosomal reformation disruptions.During my thesis, I showed that loss of spatacsin function induces lipid accumulation in lysosomesand articularly in autolysosomes both in fibroblasts and neurons from Spg11-/- mice. Gangliosidesand cholesterol are among lipids that accumulate in autolysosomes impairing lysosomal membranerecycling by disrupting the recruitment of keys roteins. Neurons with ganglioside accumulationsare more sensitive to glutamate induced neuronal death, suggesting that these accumulations areinvolved in neurodegeneration. These results could be of great importance since accumulations ofgangliosides in lysosomes arise in many diseases.I also showed that loss of spatacsin disrupts extracellular calcium import by the store-operatedcalcium entry (SOCE) leading to an increase in cytosolic calcium levels. Lysosomal calcium contentis also increased in Spg11-/- cells and calcium release from lysosome by TRPML1 is reduced.Inhibiting SOCE and stimulating lysosomal calcium release by TRPML1 reduced lipidsaccumulations in lysosomes and artially restored lysosome reformation.Our data suggest that absence of spatacsin is responsible for a disruption of calcium homeostasisthat contributes to lipid accumulation in autolysosomes, disturbing reformation of lysosomes fromautolysosomes. Inhibiting gangliosides synthesis could be used as a therapeutic strategy. However,understanding how loss of function of spatacsin alters these cellular athways will allow thedevelopment of targeted therapeutic approaches
Nakano, Makoto. "Frequency-dependent requirement for calcium store-operated mechanisms in induction of homosynaptic long-term depression at hippocampus CA1 synapses". Kyoto University, 2004. http://hdl.handle.net/2433/145290.
Texto completoSawamura, Seishirou. "Elucidation of signal regulation by interacting molecules and proteins of Ca2+ influx channels". 京都大学 (Kyoto University), 2016. http://hdl.handle.net/2433/215579.
Texto completoDeng, Xiaoxiang. "Dissecting the mechanism of STIM coupling to Orai". Diss., Temple University Libraries, 2011. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/213111.
Texto completoPh.D.
Store-operated Ca2+ entry (SOCE) triggered by the depletion of endoplasmic reticulum (ER) luminal Ca2+ stores is a major Ca2+ entry pathway in non-excitable cells and is essential in physiological Ca2+ signaling and homeostasis. STIM proteins are sensors of ER luminal Ca2+, which translocate to ER-plasma membrane (PM) junctional regions to activate the family of Orai channels mediating Ca2+ entry. This study is focused on dissecting the mechanism of STIM interacting with Orai. A powerful modifier of SOCE, 2-aminoethoxydiphenyl borate (2-APB) is utilized. First, the action of 2-APB on the mammalian Orai homologues are characterized using the DT40 STIM knockout cells. 50 ìM 2-APB directly activates Orai3 but not Orai1 or Orai2. Second, while it stimulates the STIM2-mediated constitutive Ca2+ entry through Orai, 2-APB also induces the cytosolic STIM C-terminus fragments to translocate to the PM and activate Orai1. These data reveal 50 ìM 2-APB enhances STIM-Orai coupling. Further, this enhanced binding of STIM and Orai leads to a conformational change within the STIM-Orai complex, which is possibly the underlying mechanism for the 50 ìM 2-APB inhibitory effect on SOCE. Finally, six residues (344-349) at the N-terminus of the STIM-Orai activation region (SOAR) prove to be critical for this inhibitory action. These same six amino acid region also constitutes an ancillary Orai binding site within SOAR, in addition to the main polybasic region. The deletion of this ancillary site abolishes the ability of SOAR to bind to and activate Orai1, but can be compensated for by the STIM-Orai binding enhancing effect of 50 ìM 2-APB. The majority of STIM1 is located on the ER membrane, while a small proportion of STIM1 is on the PM. Using an extracellularly applied STIM1 antibody, the PM STIM1 can be aggregated to exert an influence on the ER STIM1. Although the PM STIM1 is not obligatory for STIM1-mediated Orai activation, it nevertheless may have a functional presence in the PM. Lastly, a regulatory link between voltage-gated Ca2+ channels (Cav channels) and the STIM proteins is established. After activation by store depletion, STIM strongly suppresses the Cav1.2 channels. There is a biochemical interaction between STIM1 and the Cav1.2 pore subunit á1C. This inhibitory effect is independent of Orai1 activation. Hence, STIM1 interacts with and reciprocally controls two major Ca2+ channels.
Temple University--Theses
Beesetty, Pavani. "Consequences of TRPM7 kinase inactivation in immune cells". Wright State University / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=wright1526406780596661.
Texto completoXu, Yanjun [Verfasser], Ronald P. [Akademischer Betreuer] [Gutachter] Kühnlein y Ahmed [Gutachter] Mansouri. "Regulation of Drosophila melanogaster body fat storage by store-operated calcium entry / Yanjun Xu ; Gutachter: Ronald P. Kühnlein, Ahmed Mansouri ; Betreuer: Ronald P. Kühnlein". Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2017. http://d-nb.info/1132813042/34.
Texto completoTian, Geng. "On the Generation of cAMP Oscillations and Regulation of the Ca2+ Store-operated Pathway in Pancreatic Islet α- and β-cells". Doctoral thesis, Uppsala universitet, Institutionen för medicinsk cellbiologi, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-191852.
Texto completoGalitzine, Marie. "Redistribution des phospholipides membranaires : caractérisation des mécanismes déficients dans le syndrome hémoragique de Scott". Paris 7, 2005. http://www.theses.fr/2005PA077022.
Texto completoHenke, Nadine Verfasser], Axel [Akademischer Betreuer] Methner y Dieter [Akademischer Betreuer] [Willbold. "How Stromal Interaction Molecule 1 (STIM1) and Store Operated Calcium Entry (SOCE) affect mitochondrial energy metabolism and neuronal function / Nadine Henke. Gutachter: Axel Methner ; Dieter Willbold". Düsseldorf : Universitäts- und Landesbibliothek der Heinrich-Heine-Universität Düsseldorf, 2013. http://d-nb.info/1031074910/34.
Texto completoHenke, Nadine [Verfasser], Axel Akademischer Betreuer] Methner y Dieter [Akademischer Betreuer] [Willbold. "How Stromal Interaction Molecule 1 (STIM1) and Store Operated Calcium Entry (SOCE) affect mitochondrial energy metabolism and neuronal function / Nadine Henke. Gutachter: Axel Methner ; Dieter Willbold". Düsseldorf : Universitäts- und Landesbibliothek der Heinrich-Heine-Universität Düsseldorf, 2013. http://d-nb.info/1031074910/34.
Texto completoGoswamee, Priyodarshan. "The Role of Orai-Mediated Ca2+ Entry in Migration in a Gastroenteropancreatic Neuroendocrine Tumor Model". University of Toledo Health Science Campus / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=mco1438280470.
Texto completoLorenzo, Moldero Ivan. "Localization and regulation of trpv4 channels in CILIATED epithelia". Doctoral thesis, Universitat Pompeu Fabra, 2008. http://hdl.handle.net/10803/7185.
Texto completoClearance of mucus and pathogenic agents from lungs and the transport of gametes and embryos in the female reproductive organs are key functions of ciliated epithelia such as those present in the airways and the oviduct. The rate of mucociliary transport is a function of ciliary beat frequency (CBF) and this, in turn, is increased by increases in intracellular calcium. Transient potential vanilloid 4 (TRPV4)cation channel mediates Ca2+ influx in response to mechanical and osmotic stimuli. TRPV4 expression in ciliated epithelia from airways and oviduct is confirmed by immunofluorescence localization of the channel at the apical membrane of the polarized ciliated epithelia, where the Ca2+ signalling is required for CBF regulation. Ciliated tracheal cells from TRPV4-/-mice show no TRPV4 expression, neither increases in intracellular Ca2+ and CBF in response to the TRPV4-specific activator 4α- phorbol 12,13- idecanoate (4α-PDD), and reduced responses to mild temperatures (~25ºC - 38ºC), another TRPV4-activating stimulus. TRPV4 gating by high viscous loads and hypotonicity depends on phospholipase A2 (PLA2) pathway activation and subsequent production of epoxyeicosatrienoic acid (EET). Under conditions of low PLA2 activation, mechanical and hypotonic stimuli use extracellular ATP release-mediated activation of phospholipase C (PLC)-inositol triphosphate(IP3)signalling to support TRPV4 gating. We describe that IP3, without being an agonist itself, sensitizes TRPV4 to EET activation. Besides, the functional coupling between plasma membrane TRPV4 channels and IP3 receptors (IP3R) is required to initiate and maintain the cellular oscillatory Ca2+ signal triggered by high viscous loads and hypotonic stimuli. One of the main CBF activators, adenosine-5'-triphosphate (ATP), triggers both Ca2+ release from intracellular Ca2+ stores and Ca2+ entry. Interestingly, TRPV4 contributes to ATP-induced increase in CBF. Furthermore, our work implicates TRPV4 channel exclusively in receptor-operated Ca2+ entry. Collectively, this PhD thesis shows the role of TRPV4 channels coupling physiologically relevant mechanical, hypotonic and chemical stimuli to CBF regulation in motile ciliary epithelia.
Saul, Stephanie [Verfasser] y Markus [Akademischer Betreuer] Hoth. "Ca2+ and reactive oxygen species as determinands of immune and skin cell function$dA central role for Orai- and STIM-mediated store-operated calcium entry / Stephanie Saul. Betreuer: Markus Hoth". Saarbrücken : Saarländische Universitäts- und Landesbibliothek, 2016. http://d-nb.info/1099952107/34.
Texto completoBennett, Orville R. "Expressing human Orai3 in insect cells for pharmacological studies". Wright State University / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=wright1326846462.
Texto completoCarreras, Sureda Amado 1986. "Modulation of T lymphocite activation by ORMDL3". Doctoral thesis, Universitat Pompeu Fabra, 2014. http://hdl.handle.net/10803/319714.
Texto completoEstudis d’associació genètica ample han apuntat cap al gen ORMDL3 com a factor de risc per diverses malalties pro-inflamatòries i autoimmunes. La proteïna codificada per aquest gen pertany a una família de proteïnes transmembrana del reticle endoplàsmic involucrada en l’homeòstasi de calci i en el metabolisme lipidic cel•lular. El motiu que ens va impulsar a dur a terme aquest treball era la idea de trobar el mecanisme darrere les associacions a patologia per aquesta proteïna. Aquesta tesis explora el rol potencial d’ORMDL3 en limfòcits T, amb èmfasi al procés d’activació. Així doncs hem demostrat que la senyalització de calci i la activació de cèl•lules T es veu influenciada pels nivells d’expressió d’ORMDL3. A més hem demostrat que components del nostre genoma modifiquen els nivells d’expressió d’ORMDL3 i la fisiologia limfocitària. Per acabar hem caracteritzat el complex molecular de les proteïnes ORMDL. En conjunt, aquest treball permet una millor comprensió de la fisiopatologia associada a ORMDL3 i la seva relació amb el sistema immune
Gao, Yadong [Verfasser]. "The role of calcium-activated potassium channels and store-operated calcium channels in human macrophages / vorgelegt von Yadong Gao". 2007. http://d-nb.info/986359440/34.
Texto completoTsai, Yu-Chieh y 蔡雨潔. "The role of store-operated calcium channels in differentiation of rat mesenchymal stem cells". Thesis, 2012. http://ndltd.ncl.edu.tw/handle/20221505338518925501.
Texto completo慈濟大學
生理暨解剖醫學碩士班
100
Stem cells have certain features such as self-renewal and differentiation potential. Adult stem cells are minor populations found in adult organs, they cannot give rise to an organism and only differentiate to specific cell lineages, mesenchymal stem cells (MSC) belong to this group. MSC can differentiate into several lineages, including osteocytes, chondrocytes and adipocytes. Recently, unexpected plasticity has been attributed to mesenchymal stem cells, as they have been demonstrated to differentiate into a number of non-mesoderm-type cells such as cardiomyocytes and neuron cells. In this study, we induce rat MSC (rMSC) to differentiate into neuron-like cells and adipocytes to investigate the correlation between calcium and cell differentiation. Calcium, a ubiquitous second messenger, regulates many cellular functions, including cell growth, differentiation, and apoptosis. Intracellular calcium homeostasis is maintained via calcium channels, calcium pumps and calcium exchangers. Store-operated calcium entry (SOCE) are the major source of intracellar calcium in non-excitable cells. Therefore, the aim of this study is to investigate the role of SOC channels in rMSC differentiation. rMSC is induced to differentiate into adipocytes and neuron-like cells. We measure the difference of concentration between Control and differentiation groups using microspectrofluorometry. We find that calcium influx through SOC channels and calcium depletion is significantly increase in differentiated rMSC. Therefore, we use Western blot and Q-PCR to determene that whether the expressions of STIM-1, Orai-1 and TRPC1 is differences between Control and differentiation groups. Our finding show that the levels of STIM-1 expression is significantly increase, but the levels of Orai-1 and TRPC1 expression have no significant difference between Control and differentiation groups. Inhibition of SOCE by a treatment with 2APB can blocked rMSC differentiation. Next, we measured the expression of IP3R1, IP3R2 and IP3R3 and find a significantly increase in IP3R2 after differentiation. Our results suggest that STIM-1 may play a critical role in the differentiation process.