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Walsh, Ciara. "The regulation of STIM1 translocation to the plasma membrane". Thesis, University of Liverpool, 2010. http://livrepository.liverpool.ac.uk/1482/.
Pełny tekst źródłaTroupes, Constantine. "The Role of STIM1 in Hypertrophy-Related Contractile Dysfunction". Diss., Temple University Libraries, 2016. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/403786.
Pełny tekst źródłaPh.D.
Increases in cardiac afterload caused by disease conditions results in remodeling of heart structure by hypertrophy and alterations in the molecular regulation of contractile performance. These adaptations can be regulated by various Ca2+-dependent signaling processes. STIM1 is an important regulator of Ca2+ signaling in different cell types by sensing endoplasmic reticular Ca2+ levels and coupling to plasma membrane Orai channels. The role of STIM1 in heart is not well understood, given the robust Ca2+ regulatory machinery present within cardiac myocytes. Previous reports indicate that STIM1 may play a role in regulation of cardiac hypertrophy. The goal of this work is to understand how STIM1 can affect contractile Ca2+ regulation in normal and diseased myocytes. We induced cardiac hypertrophy by slow progressive pressure overload in adult cats. Isolated adult feline ventricular myocytes (AFMs) exhibited increased STIM1 expression and activity, which correlated with altered Ca2+ handling. Use of BTP2 to block Orai channels resulted in a reduction of action potential (AP) duration and diastolic spark rate of hypertrophied myocytes, without affecting myocytes from sham-operated animals. Overexpressed STIM1 in cultured AFMs caused persistent Ca2+ influx that resulted in increased diastolic spark rates and prolonged APs, similar to myocytes from banded animals. STIM1 mediated Ca2+ influx could load the sarcoplasmic reticulum and activated CaMKII, which increased spark rates and lead to spontaneous APs. Importantly, STIM1 operated by associating with Orai channels because these effects could be blocked with either BTP2 or with a dominant negative Orai construct. Prolonged Ca2+ entry through this pathway eventually causes cell death. In conclusion, the work presented in this thesis establishes a role for STIM1-Orai in contractile Ca2+ regulation.
Temple University--Theses
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
Frappier, Maude. "MURC est un partenaire d’interaction de STIM1 impliqué dans la signalisation calcique". Mémoire, Université de Sherbrooke, 2015. http://hdl.handle.net/11143/8332.
Pełny tekst źródłaLur, 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 źródłaSaliba, Youakim. "Identification des partenaires de STIM1 dans le cœur normal et hypertrophié". Paris 6, 2012. http://www.theses.fr/2012PA066541.
Pełny tekst źródłaWe previously showed an important role of STIM1 in cardiac hypertrophy; however, the identity of the channels responsible for the STIM1 dependent pro-hypertrophic Ca2+ entry in the rat ventricular myocytes remains to be elucidated. In this study we developed a new method of myocardial non viral gene delivery, by using the combination of ultrasound energy (USE), liposomes and high pressure injections to the rat heart. Due to its simplicity, low toxicity and low immunogenicity, this method produced sufficient number of transfected cells to perform biochemical experiments and single cell physiological measurements. We then characterized the expression profile of TRPCs and ORAIs proteins in both normal and hypertrophied ventricular myocytes, and found an upregulation of TRPC1 in hypertrophied cells. We further used the new gene delivery method to identify and screen for the STIM1 associated channel candidates via RNA interference. We identified TRPC5 as a non-selective Ca2+ channel that operates constitutively in basal conditions with increased activity in cardiac hypertrophy, as well as ORAI3 that functions in both modes: SOCE and constitutive basal Ca2+ entry in concordance with TRPC5. We developed an efficient non-viral cardiac gene delivery which we used to elucidate TRPC5 and ORAI3 as new voltage independent STIM1 regulated Ca2+ channels in the ventricular rat myocytes
Premsler, Thomas [Verfasser], Albert [Akademischer Betreuer] Sickmann i Jan Georg [Gutachter] Hengstler. "Mass spectrometry based interaction study of the STIM1 and VASP proteins : (Massenspektrometrie-basierte Interaktionsstudie der Proteine STIM1 und VASP) / Thomas Premsler. Betreuer: Albert Sickmann. Gutachter: Jan Georg Hengstler". Dortmund : Universitätsbibliothek Dortmund, 2012. http://d-nb.info/1110892373/34.
Pełny tekst źródłaCao, Hang [Verfasser]. "Effect of STIM1/2 and of Ceritinib on Platelet Function / Hang Cao". Tübingen : Universitätsbibliothek Tübingen, 2021. http://d-nb.info/1234450763/34.
Pełny tekst źródłaMukherjee, Sreya. "Applications of Molecular Modelling and Structure Based Drug Design in Drug Discovery". Scholar Commons, 2016. http://scholarcommons.usf.edu/etd/6331.
Pełny tekst źródłaMaues, de Paula André. "Pour une meilleure compréhension de la myopathie à agrégats tubulaires". Thesis, Aix-Marseille, 2016. http://www.theses.fr/2016AIXM5056.
Pełny tekst źródłaMyopathy with tubular aggregates (MTA) is a rare disease characterized by the presence of tubular aggregates in muscle biopsy. We found 15 cases of MAT in our registry including 13987 muscle biopsies performed over 35 years. Among them, there was a family of three patients that did not fit any of the previously described clinical groups of MTA, since they were asymptomatic with isolated hyperCKemia and positive contracture test. Our works revealed heterozygous mutations in the gene STIM1. These mutations localized in the gene portion that codes for the intraluminal EF-hand domain, leads to a constitutive activation of STIM1 with SOCE mecanism enhancement and consequent increase of the Ca2+ entry which was demonstrated using transfected myoblasts. We also revealed the mutation p.Arg304Trp in the coding sequencing of the CC1 domain of STIM1, as the cause of Stormorken syndrome. This fact increases the phenotypical spectra of the mutations for this gene.The results of our proteomic analysis show that the proteostasis in MTA is disturbed, because the proteome profile is different in total muscle of the patients and in their tubular aggregates when compared to controls. The enriched proteins belong to the biological pathways linked to ionic homeostasis, membrane systems of the triads and the exosome, and to the mitochondrial metabolism.Our works bring perspectives for the continuation of our studies, in order to better understand the physiopathology of the myopathy with tubular aggregates and propose efficacious therapeutic solutions
Ritchie, Michael. "TRANSCRIPTIONAL AND MOLECULAR CONTROL OF CALCIUM SIGNALING". Diss., Temple University Libraries, 2012. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/211071.
Pełny tekst źródłaPh.D.
The extensive relationship between modulation of intracellular Ca2+ content and the control of cell proliferation (Boynton et al. 1974; Whitfield et al. 1979; Berridge and Irvine 1984), differentiation (Bridges et al. 1981; Holliday et al. 1991) and death (Orrenius et al. 2003) has led to much examination into the relationship between Ca2+ signaling pathways and the onset of various pathological conditions, including cancer, cardiac hypertrophy, immunodeficiency, neurodegeneration. Control of Ca2+ signals is achieved via an extensive combination of pumps, channels and exchangers which regulate the concentration of Ca2+ within not only the cytosol but also all intracellular compartments. Accordingly, a great deal of research has focused on the mechanisms which regulate these channels and pumps, and recently the primary mechanism for Ca2+ influx in non-excitable cells has been identified. This process, termed Store-operated calcium entry (SOCe), is a key evolutionarily conserved mechanism whereby decreases in endoplasmic reticulum Ca2+ content (sensed by the ER Ca2+ sensor, STIM1) leads to the influx of Ca2+ across the plasma membrane through the Orai family of Ca2+ channels. However, many questions remain about how this Ca2+ signaling pathway is regulated. In this thesis, I provide evidence regarding the transcriptional and molecular mechanisms regulating SOCe. Initial studies in my thesis work aimed to identify some of the key events leading to dysregulation of Ca2+ homeostasis in the kidney specific pediatric malignancy, Wilms' Tumor. I found that STIM1 expression levels and SOCe signals are significantly reduced in Primary Wilms' Tumor samples. Subsequent analysis of these phenomena led me to the finding that STIM1 expression is under the control of the transcription factors Wilms' Tumor Suppressor 1 (WT1) and Early Growth Response 1 (EGR1). Subsequent investigations were carried out with the purpose to assess how activation of the EGR1 transcription factor alters long term Ca2+ signals. Indeed, I found that receptor-mediated activation of EGR1 leads to induction of STIM1 expression and increases in SOCe. However, unexpectedly through these analyses, I propose a novel role for STIM1 that STIM1 interacts with the Plasma Membrane Ca2+ ATPase (PMCA) through its C-terminal proline-rich domain and reduces PMCA-mediated Ca2+ clearance, effectively creating local, augmented Ca2+ gradients. This coordinated control of Ca2+ entry and exit from the cell has wide-ranging implications for Ca2+ signaling in multiple cell types.
Temple University--Theses
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.
Onodera, Kaoru [Verfasser]. "STIM1-regulierter Ca2+-Einstrom durch die apikale und die basolaterale Membran im Kolonepithel / Kaoru Onodera". Gießen : Universitätsbibliothek, 2013. http://d-nb.info/1064992153/34.
Pełny tekst źródłaCabanas, 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
Kato, Kenta. "Characterization of bioactive molecules using genetically engineered ion channels". 京都大学 (Kyoto University), 2010. http://hdl.handle.net/2433/120897.
Pełny tekst źródłaSamakai, Elsie. "TRANSCRIPTIONAL CONTROL OF Ca2+ SIGNALING IN T CELLS". Diss., Temple University Libraries, 2017. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/466164.
Pełny tekst źródłaPh.D.
Antigen presentation to T cells results in their activation through T Cell Receptor (TCR) stimulation, resulting in sustained elevation of cytosolic Ca2+ concentration critical for T cell activation. Sustained Ca2+ signals are important for the activation of Nuclear Factor of Activated T cells (NFAT), which is a key regulator of T cell activation through its transcriptional control of genes in multiple process including cytokine production, proliferation and differentiation(Rao, Luo, & Hogan, 1997). Recently it was shown that Stromal Interaction Molecule 1 (STIM1) inhibits plasma membrane Ca2+/ATPase 4 (PMCA4) function during T cell activation resulting in sustained elevation of Ca2+ signals(Ritchie, Samakai, & Soboloff, 2012). This interaction requires upregulation of both STIM1 and PMCA4. In this thesis, I hypothesize that changes in Ca2+ signals arising from transcriptional changes of STIM1 and PMCA are important for the efficient activation of T cells. In the first part of this thesis, I assess the transcriptional regulation of STIM1 and PMCA4. My in vitro studies show that expression of both proteins is regulated by the EGR family members, EGR1 and EGR4. Additionally, transcriptional regulation of PMCA inhibition by EGR1 and EGR4 is required for efficient activation of T cells. Interestingly, whereas significant roles for EGR1, EGR2 and EGR3 in T cell development and function have been established, a role for EGR4 has not, hitherto been elucidated. In the second half of this thesis, using qPCR, I reveal that EGR4 expression is stimulated by TCR engagement in primary double positive, CD4 and CD8 positive murine T cells. Further, EGR4-null mice exhibit shifts in early thymic development, although this does not affect the relative number of double or single positive T cells in the thymus. Interestingly, EGR4-null primary T cells exhibit normal Ca2+ entry, but fail to exhibit activation-induced inhibition of Ca2+ clearance. Although not all subsets of EGR1 and EGR4 null primary T cells exhibited decreased STIM1 expression, significant defects in proliferation, migration and/or cytokine production were observed upon stimulation in all populations, albeit to different extents. These findings reveal a two-faceted role in which EGRs regulate T cell development and function through both Ca2+-dependent and independent methods. I believe that these findings have important implications towards the general understanding of transcriptional control of Ca2+ signaling, as well as having a possible impact in the quest to advance therapies targeting immunological disorders.
Temple University--Theses
Hasegawa, Yoshinori, Masahiro Sokabe, Mitsuo Sato, Masashi Kondo, Hiromichi Aso, Satoru Ito i Nobukazu Suganuma. "STIM1 Regulates Platelet-Derived Growth Factor-Induced Migration and Ca2+ Influx in Human Airway Smooth Muscle Cells". Thesis, PLOS ONE, 2012. http://hdl.handle.net/2237/18819.
Pełny tekst źródłaTohidi-Esfahani, Ibrahim. "Molecular profiling and characterisation of the procoagulant platelet subpopulation". Thesis, The University of Sydney, 2022. https://hdl.handle.net/2123/29642.
Pełny tekst źródłaKeeley, Tyler S. "Investigating the Roles of Fucosylation and Calcium Signaling in Melanoma Invasion". Scholar Commons, 2018. https://scholarcommons.usf.edu/etd/7535.
Pełny tekst źródłaChung, Shan-Hua [Verfasser], i Matthias [Akademischer Betreuer] Seedorf. "Mechanisms of STIM1-mediated endoplasmic reticulum-plasma membrane (ER-PM) contact formation / Shan-Hua Chung ; Betreuer: Matthias Seedorf". Heidelberg : Universitätsbibliothek Heidelberg, 2014. http://d-nb.info/1180032667/34.
Pełny tekst źródłaLuik, 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.
Pełny tekst źródłaLatour, Simon. "Rôle des protéines Orai1 et STIM1 dans les lymphomes B non-Hodgkiniens, établissement d'un modèle d'étude en 3D". Thesis, Bordeaux, 2018. http://www.theses.fr/2018BORD0038.
Pełny tekst źródłaB-cell non-Hodgkin lymphomas (BNHL) are the most common hematological malignancies, usually treated with a combination of chemotherapy and anti CD20 immunothérapie. However, 40% of patients are resistant or relapse after treatment. These therapeutic failures could be due to 1) lack of therapeutic targets implicated in several oncogenic processes, 2) lack of relevant preclinical BNHL models for drug screening and lymphomagenesis studies. Calcium is an essential second messenger involved in various cell functions. In B cells, calcium entry is mainly due to Orai1 and STIM1 proteins, both of which have been associated with oncogenesis on solid tumors. However, their role in lymphomagenesis still remains to be elucidated. Our work shows that calcium signaling in BNHL cells participates in cell death induced by GA101, a novel anti-CD20 monoclonal antibody. We also demonstrate that Orai1 and STIM1 play a role in BNHL cell migration. Interestingly, both proteins controlled cell migration in a calcium-independent manner, suggesting a new role for these proteins. Finally, using cellular capsule technology, we established a new BNHL 3D model mimicking tumoral niche by including extracellular matrix and stromal cells. This new model could be used for drug screening and understanding lymphomagenesis. In summary, this work suggests that targeting of Orai1 and STIM1 is promising for BNHL treatment
Debant, Marjolaine. "Etude de la dérégulation des entrées calciques du lymphocyte B de leucémie lymphoïde chronique : mise en évidence d'une nouvelle piste thérapeutique". Thesis, Brest, 2017. http://www.theses.fr/2017BRES0150.
Pełny tekst źródłaChronic lymphocytic leukemia (CLL) is the most common hematological malignancy in Western countries and is a result of the accumulation of mature monoclonal B lymphocytes (B-CLL) carrying the CD5 glycoprotein. The B-CLL are also characterized by an alteration of calcium homeostasis with, on the one hand, the demonstration of calcium-controlled survival factors such as phospho-ERK, NFAT- 2 and IL-10, and on the other hand by a progression of the disease which is associated with the response to calcium. Initially, in order to better understand the impact of the CD5 molecule on calcium deregulations, it has been shown that the introduction of an expression plasmid for CD5 into human B cell lines was accompanied by a calcium entry in the basal state. Then, this entry, called constitutive entry, was sought in the B-CLL to show that it characterized untreated patients in the evolution phase.As with CD5 B cell lines, this new calcium entry pathway is autonomous and independent of the classical B-CLL signaling pathway: BCR-IP3R. The study of the proteins responsible for this influx made it possible to highlight, firstly three partners (STIM1, Orai1 and TRPC1), and secondly the importance of the membrane fraction of STIM1 (STIMPM) since the use of a human monoclonal antibody (mAb) anti-STIM1 is able to inhibit the constitutive entry of calcium which in turn acts on the survival of B-CLL, for STIMPM positive patients, when the anti-STIM1 mAb was used in combination with rituximab, a therapeutic anti-CD20 mAb. Finally, the modeling of the C-terminal part of STIM1 makes it possible to envisage several potential targets for the development of new anti-STIM1 mAbs. In conclusion, the introduction by the CLL malignant clone of a constitutive entry of calcium favors its aggressiveness and thus constitutes a new therapeutic pathway controllable by the use of anti-STIM1 mAb, which opens new perspectives like diagnostic and therapeutic tools
Dramane, Gado. "Etude de la signalisation calcique dans les cellules gustatives lipidiques chez la souris". Thesis, Dijon, 2012. http://www.theses.fr/2012DIJOS035/document.
Pełny tekst źródłaThe lipid-binding glycoprotein CD36, expressed by circumvallate papillae (CVP) of the mouse tongue, has been shown to be implicated in oro-gustatory perception of dietary lipids. We demonstrate that linoleic acid (LA) by activating sPLA2, cPLA2 and iPLA2 via CD36, produced arachidonic acid (AA) and lyso-phosphatidylcholine (Lyso-PC) which triggered Ca2+ influx in CD36-positive taste bud cells (TBC), purified from mouse CVP. LA induced the production of Ca2+ influx factor (CIF). CIF, AA and Lyso-PC exerted different actions on the opening of store-operated Ca2+ (SOC) channels, constituted of Orai proteins and regulated by STIM1, a sensor of Ca2+ depletion in the endoplasmic reticulum. We used siRNA technology and transgenic mice models and observed that CIF and Lyso-PC opened Orai1 channels whereas AA-opened Ca2+ channels were composed of Orai1/Orai3. STIM1 was found to regulate LA-induced CIF production and opening of both kinds of Ca2+ channels. Furthermore, Stim1–/– mice lost the spontaneous preference for fat, observed in wild-type animals. The CD36-positive TBC from Stim1–/– mice also failed to release serotonin into extracellular environment. Our results suggest that fatty acid-induced Ca2+ signaling, regulated by STIM1 via CD36, might be implicated in oro-gustatory perception of dietary lipids and the spontaneous preference for fat
Usui, Ryota. "GPR40 activation initiates store-operated Ca²⁺ entry and potentiates insulin secretion via the IP3R1/STIM1/Orai1 pathway in pancreatic β-cells". Kyoto University, 2020. http://hdl.handle.net/2433/253196.
Pełny tekst źródłaGueder, 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". Electronic Thesis or Diss., Amiens, 2018. http://www.theses.fr/2018AMIE0033.
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
Peche, Georges Arielle. "Physiopathologie de la myopathie à agrégats tubulaires". Thesis, Strasbourg, 2017. http://www.theses.fr/2017STRAJ008/document.
Pełny tekst źródłaTubular aggregate myopathy (TAM) is a genetic disorder characterized by tubular aggregates in muscle biopsies of patients. Our team identified for the first time mutations in STIM1 as causative of this disease. STIM1 (stromal interaction molecule 1) is the main calcium (Ca2+) sensor of the endo/sarcoplasmic reticulum (ER/SR). Following Ca2+ depletion of the ER/SR, STIM1 unfolds, oligomerizes and migrates close to the plasma membrane (PM) to activate the Ca2+ channel ORAI1, leading to Ca2+ entry. This mechanism is the «store-operated Ca2+ entry» (SOCE). Several teams report a mutation in STIM1 (p.R304W) leading to TAM associated with other symptoms, described as Stormorken syndrome. Therefore, this work aims to assess and compare the impact of TAM and Stormorken mutations at different stages of the SOCE pathway. We show that TAM and Stormorken mutations lead to an increase expression of the protein, a constitutive STIM1 clustering near the PM, to ORAI1 constitutive recruitment and to the activation of a Ca2+ -dependent pathway: the NFAT pathway
Huang, Yun. "Integration of Extracellular and Intracellular Calcium Signals: Roles of Calcium-Sensing Receptor (CASR), Calmodulin and Stromal Interaction Molecule 1 (STIM1)". Atlanta, Ga. : Georgia State University, 2008. http://digitalarchive.gsu.edu/chemistry_diss/28/.
Pełny tekst źródłaTitle from title page (Digital Archive@GSU, viewed July 1, 2010) Jenny J. Yang, committee chair; Edward Brown, Giovanni Gadda, Zhi-ren Liu, committee members. Includes bibliographical references (p. 230-258).
Ramanujam, Deepak Prabhu [Verfasser], Martin [Akademischer Betreuer] Klingenspor i Stefan [Akademischer Betreuer] Engelhardt. "Characterization of stromal interaction molecule 1 (STIM1) in the myocardium / Deepak Prabhu Ramanujam. Betreuer: Martin Klingenspor. Gutachter: Stefan Engelhardt ; Martin Klingenspor". München : Universitätsbibliothek der TU München, 2013. http://d-nb.info/1079001891/34.
Pełny tekst źródłaCordero, Sanchez Celia. "Characterization of a mouse model for Tubular Aggregate Myopathy and development of small molecules". Doctoral thesis, Università del Piemonte Orientale, 2022. https://hdl.handle.net/11579/148545.
Pełny tekst źródłaMariotti, Valeria. "Molecular pathophysiology of cholangiopathies: lessons from polycystic and fibropolycystic liver disease". Doctoral thesis, Università degli studi di Padova, 2019. http://hdl.handle.net/11577/3422326.
Pełny tekst źródłaCastro, Kraftchenko Joel, i 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.
Pełny tekst źródłaCastiblanco, Adriana P. "Expression and Purification of Engineered Calcium Binding Proteins". Digital Archive @ GSU, 2009. http://digitalarchive.gsu.edu/chemistry_theses/20.
Pełny tekst źródłaNguyen, Nathalie. "Régulation négative de l'activité des canaux calciques : identification de deux nouveaux frins biologiques". Thèse, Université de Sherbrooke, 2013. http://hdl.handle.net/11143/6248.
Pełny tekst źródłaEylenstein, Anja [Verfasser], i Florian [Akademischer Betreuer] Lang. "Regulierung des speicherabhangigen Ca2+-Kanals Orai1 und des Ca2+-sensitiven Proteins STIM1 durch die Serum- und Glukokortikoid induzierbare Kinase 1 / Anja Eylenstein ; Betreuer: Florian Lang". Tübingen : Universitätsbibliothek Tübingen, 2011. http://d-nb.info/1160309620/34.
Pełny tekst źródłaHenke, Nadine Verfasser], Axel [Akademischer Betreuer] Methner i 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.
Pełny tekst źródłaHenke, Nadine [Verfasser], Axel Akademischer Betreuer] Methner i 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.
Pełny tekst źródłaCohen-Aubart, Fleur. "Rôle de la protéine STIM1 sur la fonction des cellules musculaires vaculaires et cardiaques par modulation de la voie de signalisationcalcineurine-NFAT : implications physiopathologiques et pharmacologiques". Paris 6, 2012. http://www.theses.fr/2012PA066169.
Pełny tekst źródłaTian, 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.
Pełny tekst źródłaDramane, Gado, i Gado Dramane. "Etude de la signalisation calcique dans les cellules gustatives lipidiques chez la souris". Phd thesis, Université de Bourgogne, 2012. http://tel.archives-ouvertes.fr/tel-00833888.
Pełny tekst źródłaArunachalam, 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.
Pełny tekst źródłaAbdoul-Azize, Souleymane. "Implication de la signalisation calcique et des MAP kinases dans la perception gustative lipidique". Phd thesis, Université de Bourgogne, 2013. http://tel.archives-ouvertes.fr/tel-01018378.
Pełny tekst źródłaTerrie, 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.
Pełny tekst źródłaNeural 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
Pancaldi, Marco. "Stime satellitari di stabilità atmosferica". Bachelor's thesis, Alma Mater Studiorum - Università di Bologna, 2019. http://amslaurea.unibo.it/18271/.
Pełny tekst źródłaCesarini, Ettore. "Stima streaming di sottospazi principali". Master's thesis, Alma Mater Studiorum - Università di Bologna, 2019. http://amslaurea.unibo.it/17897/.
Pełny tekst źródłaDotti, Michele. "Stima dell'assetto di un UAV". Bachelor's thesis, Alma Mater Studiorum - Università di Bologna, 2014. http://amslaurea.unibo.it/6362/.
Pełny tekst źródłaCiaroni, Riccardo. "Stima dello stato nelle reti di distribuzione". Master's thesis, Alma Mater Studiorum - Università di Bologna, 2018. http://amslaurea.unibo.it/17249/.
Pełny tekst źródłaVenieri, Laura. "Stime subellittiche per operatori somma di quadrati". Bachelor's thesis, Alma Mater Studiorum - Università di Bologna, 2011. http://amslaurea.unibo.it/2345/.
Pełny tekst źródłaLinguerri, Matteo. "Stima della portata cardiaca dalla pressione aortica". Bachelor's thesis, Alma Mater Studiorum - Università di Bologna, 2013. http://amslaurea.unibo.it/6386/.
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