Bibliografías temáticas / STIM1

Literatura académica sobre el tema "STIM1"

Autor: Grafiati
Publicado: 4 de junio de 2021
Última modificación: 1 de junio de 2024

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Artículos de revistas sobre el tema "STIM1"

1

WILLIAMS, Richard T., Shehnaaz S. M. MANJI, Nigel J. PARKER, Manuela S. HANCOCK, Leonie van STEKELENBURG, Jean-Pierre EID, Paul V. SENIOR et al. "Identification and characterization of the STIM (stromal interaction molecule) gene family: coding for a novel class of transmembrane proteins". Biochemical Journal 357, n.º 3 (25 de julio de 2001): 673–85. http://dx.doi.org/10.1042/bj3570673.

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STIM1 (where STIM is stromal interaction molecule) is a candidate tumour suppressor gene that maps to human chromosome 11p15.5, a region implicated in a variety of cancers, particularly embryonal rhabdomyosarcoma. STIM1 codes for a transmembrane phosphoprotein whose structure is unrelated to that of any other known proteins. The precise pathway by which STIM1 regulates cell growth is not known. In the present study we screened gene databases for STIM1-related sequences, and have identified and characterized cDNA sequences representing a single gene in humans and other vertebrates, which we have called STIM2. We identified a single STIM homologue in Drosophila melanogaster (D-Stim) and Caenorhabditis elegans, but no homologues in yeast. STIM1, STIM2 and D-Stim have a conserved genomic organization, indicating that the vertebrate family of two STIM genes most probably arose from a single ancestral gene. The three STIM proteins each contain a single SAM (sterile α-motif) domain and an unpaired EF hand within the highly conserved extracellular region, and have coiled-coil domains that are conserved in structure and position within the cytoplasmic region. However, the STIM proteins diverge significantly within the C-terminal half of the cytoplasmic domain. Differential levels of phosphorylation appear to account for two molecular mass isoforms (105 and 115kDa) of STIM2. We demonstrate by mutation analysis and protein sequencing that human STIM2 initiates translation exclusively from a non-AUG start site in vivo. STIM2 is expressed ubiquitously in cell lines, and co-precipitates with STIM1 from cell lysates. This association into oligomers in vivo indicates a possible functional interaction between STIM1 and STIM2. The structural similarities between STIM1, STIM2 and D-STIM suggest conserved biological functions.
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2

Cully, Tanya R., Joshua N. Edwards, Oliver Friedrich, D. George Stephenson, Robyn M. Murphy y Bradley S. Launikonis. "Changes in plasma membrane Ca-ATPase and stromal interacting molecule 1 expression levels for Ca2+ signaling in dystrophic mdx mouse muscle". American Journal of Physiology-Cell Physiology 303, n.º 5 (1 de septiembre de 2012): C567—C576. http://dx.doi.org/10.1152/ajpcell.00144.2012.

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The majority of the skeletal muscle plasma membrane is internalized as part of the tubular (t-) system, forming a standing junction with the sarcoplasmic reticulum (SR) membrane throughout the muscle fiber. This arrangement facilitates not only a rapid and large release of Ca2+ from the SR for contraction upon excitation of the fiber, but has also direct implications for other interdependent cellular regulators of Ca2+. The t-system plasma membrane Ca-ATPase (PMCA) and store-operated Ca2+ entry (SOCE) can also be activated upon release of SR Ca2+. In muscle, the SR Ca2+ sensor responsible for rapidly activated SOCE appears to be the stromal interacting molecule 1L (STIM1L) isoform of STIM1 protein, which directly interacts with the Orai1 Ca2+ channel in the t-system. The common isoform of STIM1 is STIM1S, and it has been shown that STIM1 together with Orai1 in a complex with the partner protein of STIM (POST) reduces the activity of the PMCA. We have previously shown that Orai1 and STIM1 are upregulated in dystrophic mdx mouse muscle, and here we show that STIM1L and PMCA are also upregulated in mdx muscle. Moreover, we show that the ratios of STIM1L to STIM1S in wild-type (WT) and mdx muscle are not different. We also show a greater store-dependent Ca2+ influx in mdx compared with WT muscle for similar levels of SR Ca2+ release while normal activation and deactivation properties were maintained. Interestingly, the fiber-averaged ability of WT and mdx muscle to extrude Ca2+ via PMCA was found to be the same despite differences in PMCA densities. This suggests that there is a close relationship among PMCA, STIM1L, STIM1S, Orai1, and also POST expression in mdx muscle to maintain the same Ca2+ extrusion properties as in the WT muscle.
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3

Yoshikawa, Soichiro, Masatsugu Oh-hora, Ryota Hashimoto, Toshihisa Nagao, Louis Peters, Mayumi Egawa, Takuya Ohta et al. "Pivotal role of STIM2, but not STIM1, in IL-4 production by IL-3–stimulated murine basophils". Science Signaling 12, n.º 576 (9 de abril de 2019): eaav2060. http://dx.doi.org/10.1126/scisignal.aav2060.

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Basophils have nonredundant roles in various immune responses that require Ca2+influx. Here, we examined the role of two Ca2+sensors, stromal interaction molecule 1 and 2 (STIM1 and STIM2), in basophil activation. We found that loss of STIM1, but not STIM2, impaired basophil IL-4 production after stimulation with immunoglobulin E (IgE)–containing immune complexes. In contrast, when basophils were stimulated with IL-3, loss of STIM2, but not STIM1, reduced basophil IL-4 production. This difference in STIM proteins was associated with distinct time courses of Ca2+influx and transcription of theIl4gene that were elicited by each stimulus. Similarly, basophil-specific STIM1 expression was required for IgE-driven chronic allergic inflammation in vivo, whereas STIM2 was required for IL-4 production after combined IL-3 and IL-33 treatment in mice. These data indicate that STIM1 and STIM2 have differential roles in the production of IL-4, which are stimulus dependent. Furthermore, these results illustrate the vital role of STIM2 in basophils, which is often considered to be less important than STIM1.
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4

Skibinska-Kijek*, Anna, Marta Wisniewska, Joanna Gruszczynska-Biegala, Axel Methner y Jacek Kuznicki. "Immunolocalization of STIM1 in the mouse brain". Acta Neurobiologiae Experimentalis 69, n.º 4 (31 de diciembre de 2009): 413–28. http://dx.doi.org/10.55782/ane-2009-1753.

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Capacitative Calcium Entry (CCE) in neurons seems to depend, as in non-excitatory cells, on endoplasmic reticulum calcium sensors STIM1 or STIM2. We show localization of STIM1 in the mouse brain by immunohistochemistry with a specific antibody. STIM1 immunoreactivity has wide, but not uniform, distribution throughout the brain and is observed in neuropil and cells. The most intensive immunoreactivity is observed in Purkinje neurons of cerebellum. High/moderate levels of immunostaining are found in hippocampus, cerebral cortex and in cortico-medial amygdala, low in thalamus and basolateral amygdala. Co-staining with anti-NeuN antibody identify STIM1 immunopositive cells as neurons. Real time PCR demonstrates that Stim2 expression is 7-fold higher than that of Stim1 in hippocampus and 3-fold in other regions. Immunoblotting confirms that levels of STIMs vary in different brain regions. The data show that STIM1 and STIM2 are present in the brain, thus both can be involved in CCE, depending on neuronal type.
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5

Skopin, Anton Yu, Andrey D. Grigoryev, Lyubov N. Glushankova, Alexey V. Shalygin, Guanghui Wang, Viktor G. Kartzev y Elena V. Kaznacheyeva. "A Novel Modulator of STIM2-Dependent Store-Operated Ca2+ Channel Activity". Acta Naturae 13, n.º 1 (15 de marzo de 2021): 140–46. http://dx.doi.org/10.32607/actanaturae.11269.

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Store-operated Ca2+ entry is one of the main pathways of calcium influx into non-excitable cells, which entails the initiation of many intracellular processes. The endoplasmic reticulum Ca2+ sensors STIM1 and STIM2 are the key components of store-operated Ca2+ entry in mammalian cells. Under physiological conditions, STIM proteins are responsible for store-operated Ca2+ entry activation. The STIM1 and STIM2 proteins differ in their potency for activating different store-operated channels. At the moment, there are no selective modulators of the STIM protein activity. We screened a library of small molecules and found the 4-MPTC compound, which selectively inhibited STIM2-dependent store-operated Ca2+ entry (IC50 = 1 M) and had almost no effect on the STIM1-dependent activation of store-operated channels.
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6

Chung, Steve, MengQi Zhang y Peter Stathopulos. "The 2β Splice Variation Alters the Structure and Function of the Stromal Interaction Molecule Coiled-Coil Domains". International Journal of Molecular Sciences 19, n.º 11 (25 de octubre de 2018): 3316. http://dx.doi.org/10.3390/ijms19113316.

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Stromal interaction molecule (STIM)-1 and -2 regulate agonist-induced and basal cytosolic calcium (Ca2+) levels after oligomerization and translocation to endoplasmic reticulum (ER)-plasma membrane (PM) junctions. At these junctions, the STIM cytosolic coiled-coil (CC) domains couple to PM Orai1 proteins and gate these Ca2+ release-activated Ca2+ (CRAC) channels, which facilitate store-operated Ca2+ entry (SOCE). Unlike STIM1 and STIM2, which are SOCE activators, the STIM2β splice variant contains an 8-residue insert located within the conserved CCs which inhibits SOCE. It remains unclear if the 2β insert further depotentiates weak STIM2 coupling to Orai1 or independently causes structural perturbations which prevent SOCE. Here, we use far-UV circular dichroism, light scattering, exposed hydrophobicity analysis, solution small angle X-ray scattering, and a chimeric STIM1/STIM2β functional assessment to provide insights into the molecular mechanism by which the 2β insert precludes SOCE activation. We find that the 2β insert reduces the overall α-helicity and enhances the exposed hydrophobicity of the STIM2 CC domains in the absence of a global conformational change. Remarkably, incorporation of the 2β insert into the STIM1 context not only affects the secondary structure and hydrophobicity as observed for STIM2, but also eliminates the more robust SOCE response mediated by STIM1. Collectively, our data show that the 2β insert directly precludes Orai1 channel activation by inducing structural perturbations in the STIM CC region.
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7

Kim, Soo J., Roland R. Roy, Hui Zhong, Hideki Suzuki, Lusine Ambartsumyan, Fadia Haddad, Kenneth M. Baldwin y V. Reggie Edgerton. "Electromechanical stimulation ameliorates inactivity-induced adaptations in the medial gastrocnemius of adult rats". Journal of Applied Physiology 103, n.º 1 (julio de 2007): 195–205. http://dx.doi.org/10.1152/japplphysiol.01427.2006.

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The efficacy of high-load, short-duration isometric contractions, delivered as one vs. two sessions per day, on blunting inactivity-induced adaptations in the medial gastrocnemius (MG) were compared. Adult rats were assigned to a control (Con) or spinal cord-isolated (SI) group where one limb was stimulated (SI-Stim) while the other served as a SI control (SI-C). One bout of stimulation (BION microstimulator) consisted of a 100-Hz, 1-s stimulus, delivered every 30 s for 5 min with a 5-min rest period. This bout was repeated six times consecutively (SI-Stim1) or with a 9-h rest interval after the third bout (SI-Stim2) for 30 consecutive days. MG weights (relative to body weight) were 63, 72, and 79% of Con in SI-C, SI-Stim1, and SI-Stim2, respectively. Mean fiber size was 56% smaller in SI-C than in Con, and it was 19 and 31% larger in SI-Stim1 and SI-Stim2, respectively, compared with SI-C. Maximum tetanic tension was 42, 60, and 73% of Con in SI-C, SI-Stim1, and SI-Stim2, respectively. Specific tension was 77% of Con in SI-C, and at Con levels in both SI-Stim groups. SI increased the percent IIb myosin heavy chain composition (from 49 to 77%) and IIb+ fibers (from 63 to 79%): these adaptations were prevented by both Stim paradigms. These results demonstrate that 1) brief periods of high-load isometric contractions are effective in reducing inactivity-induced atrophy, functional deficits, and phenotypic adaptations in a fast hindlimb extensor, and 2) the same amount of stimulation distributed in two compared with one session per day is more effective in ameliorating inactivity-related adaptations.
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8

Skobeleva, Ksenia, Alexey Shalygin, Elena Mikhaylova, Irina Guzhova, Maria Ryazantseva y Elena Kaznacheyeva. "The STIM1/2-Regulated Calcium Homeostasis Is Impaired in Hippocampal Neurons of the 5xFAD Mouse Model of Alzheimer’s Disease". International Journal of Molecular Sciences 23, n.º 23 (26 de noviembre de 2022): 14810. http://dx.doi.org/10.3390/ijms232314810.

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Alzheimer’s disease (AD) is the most common cause of age-related dementia. Neuronal calcium homeostasis impairment may contribute to AD. Here we demonstrated that voltage-gated calcium (VGC) entry and store-operated calcium (SOC) entry regulated by calcium sensors of intracellular calcium stores STIM proteins are affected in hippocampal neurons of the 5xFAD transgenic mouse model. We observed excessive SOC entry in 5xFAD mouse neurons, mediated by STIM1 and STIM2 proteins with increased STIM1 contribution. There were no significant changes in cytoplasmic calcium level, endoplasmic reticulum (ER) bulk calcium levels, or expression levels of STIM1 or STIM2 proteins. The potent inhibitor BTP-2 and the FDA-approved drug leflunomide reduced SOC entry in 5xFAD neurons. In turn, excessive voltage-gated calcium entry was sensitive to the inhibitor of L-type calcium channels nifedipine but not to the T-type channels inhibitor ML218. Interestingly, the depolarization-induced calcium entry mediated by VGC channels in 5xFAD neurons was dependent on STIM2 but not STIM1 protein in cells with replete Ca2+ stores. The result gives new evidence on the VGC channel modulation by STIM2. Overall, the data demonstrate the changes in calcium signaling of hippocampal neurons of the AD mouse model, which precede amyloid plaque accumulation or other signs of pathology manifestation.
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9

Garcia-Alvarez, Gisela, Bo Lu, Kenrick An Fu Yap, Loo Chin Wong, Jervis Vermal Thevathasan, Lynette Lim, Fang Ji et al. "STIM2 regulates PKA-dependent phosphorylation and trafficking of AMPARs". Molecular Biology of the Cell 26, n.º 6 (15 de marzo de 2015): 1141–59. http://dx.doi.org/10.1091/mbc.e14-07-1222.

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STIMs (STIM1 and STIM2 in mammals) are transmembrane proteins that reside in the endoplasmic reticulum (ER) and regulate store-operated Ca2+ entry (SOCE). The function of STIMs in the brain is only beginning to be explored, and the relevance of SOCE in nerve cells is being debated. Here we identify STIM2 as a central organizer of excitatory synapses. STIM2, but not its paralogue STIM1, influences the formation of dendritic spines and shapes basal synaptic transmission in excitatory neurons. We further demonstrate that STIM2 is essential for cAMP/PKA-dependent phosphorylation of the AMPA receptor (AMPAR) subunit GluA1. cAMP triggers rapid migration of STIM2 to ER–plasma membrane (PM) contact sites, enhances recruitment of GluA1 to these ER-PM junctions, and promotes localization of STIM2 in dendritic spines. Both biochemical and imaging data suggest that STIM2 regulates GluA1 phosphorylation by coupling PKA to the AMPAR in a SOCE-independent manner. Consistent with a central role of STIM2 in regulating AMPAR phosphorylation, STIM2 promotes cAMP-dependent surface delivery of GluA1 through combined effects on exocytosis and endocytosis. Collectively our results point to a unique mechanism of synaptic plasticity driven by dynamic assembly of a STIM2 signaling complex at ER-PM contact sites.
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10

Walsh, Ciara M., Michael Chvanov, Lee P. Haynes, Ole H. Petersen, Alexei V. Tepikin y Robert D. Burgoyne. "Role of phosphoinositides in STIM1 dynamics and store-operated calcium entry". Biochemical Journal 425, n.º 1 (14 de diciembre de 2009): 159–68. http://dx.doi.org/10.1042/bj20090884.

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Ca2+ entry through store-operated Ca2+ channels involves the interaction at ER–PM (endoplasmic reticulum–plasma membrane) junctions of STIM (stromal interaction molecule) and Orai. STIM proteins are sensors of the luminal ER Ca2+ concentration and, following depletion of ER Ca2+, they oligomerize and translocate to ER–PM junctions where they form STIM puncta. Direct binding to Orai proteins activates their Ca2+ channel function. It has been suggested that an additional interaction of the C-terminal polybasic domain of STIM1 with PM phosphoinositides could contribute to STIM1 puncta formation prior to binding to Orai. In the present study, we investigated the role of phosphoinositides in the formation of STIM1 puncta and SOCE (store-operated Ca2+ entry) in response to store depletion. Treatment of HeLa cells with inhibitors of PI3K (phosphatidylinositol 3-kinase) and PI4K (phosphatidylinositol 4-kinase) (wortmannin and LY294002) partially inhibited formation of STIM1 puncta. Additional rapid depletion of PtdIns(4,5)P2 resulted in more substantial inhibition of the translocation of STIM1–EYFP (enhanced yellow fluorescent protein) into puncta. The inhibition was extensive at a concentration of LY294002 (50 μM) that should primarily inhibit PI3K, consistent with a major role for PtdIns(4,5)P2 and PtdIns(3,4,5)P3 in puncta formation. Depletion of phosphoinositides also inhibited SOCE based on measurement of the rise in intracellular Ca2+ concentration after store depletion. Overexpression of Orai1 resulted in a recovery of translocation of STMI1 into puncta following phosphoinositide depletion and, under these conditions, SOCE was increased to above control levels. These observations support the idea that phosphoinositides are not essential but contribute to STIM1 accumulation at ER–PM junctions with a second translocation mechanism involving direct STIM1–Orai interactions.
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Tesis sobre el tema "STIM1"

1

Walsh, Ciara. "The regulation of STIM1 translocation to the plasma membrane". Thesis, University of Liverpool, 2010. http://livrepository.liverpool.ac.uk/1482/.

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A rise in intracellular Ca2+ concentration is key to controlling both short term and long term Ca2+ dependent processes which include secretion, metabolism and gene expression, cell growth and proliferation. Store operated Ca2+ channels (SOCs), which are activated by the depletion of Ca2+ from internal Ca2+ stores, the main store being the endoplasmic reticulum (ER), are the major route for Ca2+ influx in non-excitable cell types. Stromal interacting molecule 1 (STIM1) is a Ca2+ sensing protein located in the endoplasmic reticulum (ER). Depletion of ER calcium stores triggers oligomerisation and subsequent translocation of STIM1 from its reticular location to specialized endoplasmic reticulum-plasma membrane (ER-PM) junctions where it forms STIM1 puncta and interacts with the SOC channel, Orai1. This induces the clustering of Orai1 into a functional tetrameric pore which is permeable to Ca2+ ions, enabling Ca2+ entry into the cell. The precise mechanism by which STIM1 is recruited to the plasma membrane to activate SOCs and the plasma membrane components involved in targeting STIM1 to the plasma membrane are largely unknown. In this study the mechanisms underlying movement of STIM1 to the plasma membrane and its accumulation at ER-plasma membrane junctions was explored in HeLa cells. In the initial part of this study I investigated whether the movement of STIM1 to the plasma membrane is an ATP-dependent process. I found that depletion of cytosolic ATP can stimulate STIM1 puncta formation in HeLa cells and that the formation of STIM1-Orai1 complexes at the plasma membrane is unaffected in these conditions. Inhibition of ATP synthesis also initiated the loss of phosphatidylinositol 4,5-bisphosphate (PtdIns(4,5)P2) from the plasma membrane. ATP depletion did not affect the structure of the microtubule cytoskeleton. These results suggest that the translocation of STIM1 and the formation of STIM1-Orai1 complexes is an ATP independent process which is not due to the disruption of microtubules and support a diffusional model for STIM1 puncta formation. It has been suggested that an additional interaction of the C-terminal polybasic domain of STIM1 with plasma membrane phosphoinositides could contribute to STIM1 puncta formation prior to binding to Orai1. I investigated the role of phosphoinositides in the formation of STIM1 puncta and SOCE in response to store depletion. Treatment of HeLa cells with inhibitors of the phosphatidylinositol 3-kinase (PI3K) and phosphatidylinositol 4-kinase (wortmannin and LY294002) partially inhibited formation of STIM1 puncta. Additional rapid depletion of PtdIns(4,5)P2 resulted in more substantial inhibition of the translocation of STIM1-EYFP into puncta. The inhibition was extensive at a concentration of LY294002 (50 μM) that should primarily inhibit PI3K consistent with a major role for PtdIns(4,5)P2 and PtdIns(3,4,5)P3 in puncta formation. Depletion of phosphoinositides also partially inhibited SOCE. Overexpression of Orai1 resulted in a recovery of translocation of STMI1 into puncta following phosphoinositide depletion and under these conditions SOCE was increased to above control levels. These observations support the idea that phosphoinositides are not essential but contribute to STIM1 accumulation at ER-PM junctions with a second translocation mechanism involving direct STIM1/Orai1 interactions. It was recently reported that STIM1 and Orai1 may function within a macromolecular complex involving other unidentified proteins. In this study I have identified that Golli-BG21, a member of the myelin basic protein (MBP) family, can directly interact with STIM1. Golli interacts with the C-terminal domain of STIM1 in both in vitro and in vivo binding assays and this interaction may be modulated by intracellular Ca2+ concentration. Golli also colocalises with full length STIM1 and Orai1 complexes in HeLa cells following store depletion. Overexpression of Golli reduces SOCE in HeLa cells but this inhibition is overcome by overexpressing STIM1. We therefore suggest that Golli binds to STIM1-Orai1 complexes to negatively regulate the activity of SOCs.
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2

Troupes, 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.

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Biomedical Sciences
Ph.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
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3

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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4

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.

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Dans les cardiomyocytes, la concentration intracellulaire de Ca2+ doit être finement régulée pour maintenir l’homéostasie calcique. La protéine Stromal interaction molecule 1 (STIM1), qui joue un rôle important dans le maintien des niveaux intracellulaires de Ca2+ des cellules non excitables en opérant l’entrée capacitative de Ca2+ (SOCE), est aussi présente dans les cardiomyocytes. Plusieurs études démontrent que STIM1 et le SOCE jouent un rôle important dans le développement de l’hypertrophie des cardiomyocytes. De plus, récemment, un nouveau rôle de STIM1 a commencé à émerger. STIM1 pourrait moduler l’expression de certains canaux calciques à la membrane plasmique en régulant leur trafic intracellulaire. Le but de l’étude était d’identifier des partenaires d’interaction de STIM1 dans l’optique de révéler le mécanisme par lequel STIM1 induit l’internalisation d’un canal calcique voltage-dépendant. Les protéines recueillies par le pull-down à partir des lysats de coeurs de rats avec une colonne d’affinité composée du domaine ERM de STIM1, ont été analysées en spectrométrie de masse. La protéine Muscle related coiled-coil (MURC), une protéine de la famille des Cavin, a été retenue comme partenaire d’interaction potentiel de STIM1. Comme elle est exprimée dans les cardiomyocytes et dans les cellules musculaires squelettiques, qui sont des cellules où la régulation de la signalisation calcique est primordiale pour le bon fonctionnement des tissus et qu’elle semble interagir avec STIM1, qui est un acteur important de la signalisation calcique, notre objectif s’est élargi et nous avons investigué sur l’implication de MURC dans la signalisation calcique en général. Nous avons donc confirmé par co-immunoprécipitation que le domaine ERM de STIM1 interagissait avec MURC. Puis, par des essais d’imagerie calcique, nous avons démontré que la surexpression de MURC pouvait provoquer différentes réponses dans différents types cellulaires en fonction de l’activation de la mobilisation calcique. En effet, nous avons observé une augmentation du SOCE qui est indépendante de la voie RhoA/ROCK dans les cellules HEK293T, une diminution de l’entrée de calcium médiée par un récepteur (ROCE) qui est pourrait être dépendante de la voie RhoA/ROCK dans les cellules T6.11 et une diminution de l’activation de RhoA de façon dépendante de l’activation du SOCE dans les cardiomyocytes HL-1. Nous avons aussi montré que MURC pouvait interagir à la membrane plasmique avec les protéines Orai1, qui sont les protéines formant les canaux CRAC (Ca2+ release-activated Ca2+) du SOCE et ce de façon dépendante de l’activation de STIM1. Enfin, les résultats de cette étude suggèrent que MURC est un partenaire d’interaction de STIM1 impliqué dans la signalisation calcique. En effet, MURC peut moduler l’activation de RhoA, ce qui pourrait induire l’internalisation de canaux calciques. De plus, son interaction avec STIM1 et Orai1 pourrait notamment faire un pont facilitant l’interaction entre STIM1 et Orai1 ce qui aurait pour effet d’augmenter le SOCE et possiblement contribuer à augmenter l’hypertrophie des cardiomyocytes.
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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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Saliba, Youakim. "Identification des partenaires de STIM1 dans le cœur normal et hypertrophié". Paris 6, 2012. http://www.theses.fr/2012PA066541.

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Nous avons déjà démontré un rôle important de STIM1 dans l’induction de l’hypertrophie cardiaque, mais l’identité des canaux STIM1 dépendants responsables de ce flux calcique pro-hypertrophique dans les cellules ventriculaires du rat reste à déterminer. Dans cette étude, nous avons développé une nouvelle méthode de transfert myocardique de gène non viral, en utilisant l’énergie des ultrasons, des liposomes et des injections pressurisées dans le myocarde du rat. Grâce à sa simplicité, son efficacité et sa faible immunogénicité, cette technique a produit un nombre suffisant de cellules transfectées pour effectuer des expériences biochimiques et physiologiques sur cellules isolées. Nous avons ensuite caractérisé le profil d’expression des protéines ORAIs et TRPCs dans les cellules ventriculaires normales et hypertrophiées, et avons trouvé une augmentation de l’expression de TRPC1 dans l’hypertrophie cardiaque. Ensuite nous avons utilisé la méthode de transfert de gènes pour identifier les partenaires canalaires de STIM1 via l’ARN interférence par injection de siARN. Nous avons identifié TRPC5 comme un canal calcique non-sélectif qui fonctionne d’une façon constitutive en conditions basales, avec une activité accrue dans l’hypertrophie cardiaque ; ainsi que ORAI3 qui opère dans deux modes: entrée capacitative de calcium et entrée constitutive en concordance avec TRPC5. Nous avons développé une nouvelle méthode de transfert myocardique de gène non viral que nous avons ensuite utilisée pour identifier TRPC5 et ORAI3 comme nouveaux canaux voltage indépendants et STIM1 dépendants dans les myocytes ventriculaires de rat
We 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
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Premsler, Thomas [Verfasser], Albert [Akademischer Betreuer] Sickmann y 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.

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Cao, Hang [Verfasser]. "Effect of STIM1/2 and of Ceritinib on Platelet Function / Hang Cao". Tübingen : Universitätsbibliothek Tübingen, 2021. http://d-nb.info/1234450763/34.

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Mukherjee, Sreya. "Applications of Molecular Modelling and Structure Based Drug Design in Drug Discovery". Scholar Commons, 2016. http://scholarcommons.usf.edu/etd/6331.

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Calcium ions have important roles in cellular processes including intracellular signaling, protein folding, enzyme activation and initiation of programmed cell death. Cells maintain low levels of calcium in their cytosol in order to regulate these processes. When activation of calcium-dependent processes is needed, cells can release calcium stored in the endoplasmic reticulum (ER) into the cytosol to initiate the processes. This can also initiate formation of plasma membrane channels that allow entry of additional calcium from the extracellular milieu. The change in calcium levels is referred to as calcium flux. A key protein involved in initiation of calcium flux is Stromal Interaction Molecule 1 (STIM1), which has recently been identified as a sensor of ER calcium levels. STIM1 is an ER transmembrane protein that is activated by a drop in ER calcium levels. Upon activation, STIM1 oligomerizes with a plasma membrane protein, ORA1, to form calcium-selective plasma membrane channels. Dysregulation of calcium flux has been reported in cancers, autoimmune diseases and other diseases. STIM1 is a promising target in drug discovery due to its key role early in calcium flux. Here we review the involvement and importance of STIM1 in diseases and we discuss STIM1 as a viable target for drug discovery using computational chemistry methods to rapidly identify new molecules to target STIM1. Herein, computational techniques were used to understand the mechanistic role of STIM1 and virtual screening is in process to discover potential inhibitors of STIM1 activity. Also mutational analysis on STIM1 was performed computationally to see the effect it had on the protein computationally. It has been found that tumor cells and tissues, compared to normal cells, have higher levels of copper and possibly other metal ions. This presents a potential vulnerability of tumor cells that can serve as a physiological difference between cancer cells and normal cells and allows design of compounds that selectively target tumor cells while sparing normal cells. Recently we have identified compounds that have potential to inhibit the proteasome in tumor cells and induce cell death by mobilizing endogenous tumor copper resulting in in cellulo activation of the compound. These compounds hence act as pro-drugs, becoming active drugs in tumor cells with high copper content but remaining essentially inactive in normal cells, thereby greatly reducing adverse effects in patients. Such use would be of significant benefit in early detection and treatment of cancers, in particular, aggressive cancers such as pancreatic cancer which is usually not detected until it has reached an advanced stage. Six compounds were identified following virtual screening of the NCI Diversity Set with our proteasome computer model followed by confirmation with a biochemical assay that showed significant inhibition of the proteasome by the compounds in the presence of copper ions. In a dose response assay, NSC 37408 (6, 7-dihydroxy-1-benzofuran-3-one), our best compound, exhibited an IC50 of 3µM in the presence of 100 nM copper. Chagas’ Disease, a parasitic disease caused by the parasite Trypanosma Cruzi, is endemic to Latin America. The disease manifests itself in a short acute phase and a long chronic phase. Current treatments are effective only in the acute phase and are not used in the chronic phase due to toxicity of the drugs. Hence a new drug discovery approach was chosen for this disease. Cruzain is the major etiologic enzyme involved in the disease and is only present in the parasite. It is also an enzyme expressed by the parasite in both phases. Herein, a novel peptoid library containing hydromethylketones was constructed and screened against a virtual structure of cruzain. The peptoids thus found through this drug discovery effort can be used as potential drug candidates against cruzain. Computational techniques will help achieve a high degree of specificity and aid in proposing assays for determining compounds with high activity Alzheimer disease is the most common form of dementia. Its pathogenesis incorporates many potential targets for treatment. Among the targets identified, Apolipoprotein E4 (apoE4) is especially interesting due to its catalytic role in the degradation and clearance of amyloid beta (Aβ), a risk factor for Alzheimer disease. ApoE exists in 3 isoforms which directly impact its functionality in the body. There are characteristic structural differences between them. In ApoE4 ionic interactions exist between Arg-61 and Glu-255 residues, unlike the other isoforms. Hence interruption of this interaction by inhibitors may change the structure of apoE4 to a more linear structure as observed in the other isoforms. Virtual screening of the NCI diversity set on an energy minimized protein virtual structure was performed to identify potential small molecule inhibitors and to gain further understanding of interactions that can be targeted to inhibit this protein. From the top ligands in the NCI diversity set, a peptide library was designed to target the protein. Previous research has indicated that liquid assisted grinding (LAG) is efficient and reliable for cocrystal formation when compared to solvent crystallization and dimethyl formamide is the best solvent for grinding. Herein, we report the comparison of four screening processes: Slurry, solvent crystallization, LAG and dry grinding. Thirty-eight crystal forms containing the Narom··· COOH, Narom···OH supramolecular heterosynthons were screened in the process, and it was observed that slurry methodology is as efficient and reliable in forming cocrystals as solution crystallization. Twenty-four new crystal forms were also isolated herein. LAG was found to be more efficient as compared to dry grinding and was successful in the formation of twenty-five crystal forms of the thirty-eight screened. Dimethyl formamide still remains the best solvent for LAG. All our slurry experiments were performed in water and it was found that water can be used reliably for this method for compounds within a wide range of solubility, thereby increasing the versatility and usability of this method for future screening procedures.
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Maues, de Paula André. "Pour une meilleure compréhension de la myopathie à agrégats tubulaires". Thesis, Aix-Marseille, 2016. http://www.theses.fr/2016AIXM5056.

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La myopathie à agrégats tubulaire (MTA) est une maladie rare caractérisée par la présence, dans la biopsie musculaire, d’« agrégats tubulaires ». Nous avons retrouvé 15 cas de MTA parmi 13987 biopsies musculaires réalisées dans les 35 dernières années dans notre service. Parmi ces cas, se trouvait une famille de trois patients qui ne pouvaient être inclus dans aucun groupe clinique connu de myopathie à agrégats tubulaires, car ils étaient asymptomatiques avec une hyperCKémie isolée et un test de contracture positif.Nos travaux ont mis en évidence des mutations hétérozygotes du gène STIM1. Ces mutations localisées dans la partie du gène qui code le domaine intraluminal EF-hand, entrainent une activation constitutive de STIM1 avec exacerbation du mécanisme SOCE et en conséquence l’augmentation de l’influx de Ca2+, démontré dans des myoblastes transfectés. Nous avons également mis en évidence la mutation p.Arg304Trp du gène STIM1, comme cause du syndrome de Stormorken. Cela augmente le spectre phénotypique des mutations de ce gène.Nos résultats de l’analyse protéomique montrent que la protéostase dans la MTA est dérégulée, car le profil du protéome est différent chez les patients et dans les agrégats tubulaires microdisséqués par laser, en comparaison a des contrôles. Les protéines enrichies s’avèrent appartenir à des voies biologiques impliquées dans l’homéostase ionique, les systèmes de membranes de la triade et de l’exosome et dans le métabolisme mitochondrial.Nos travaux ouvrent des perspectives pour mieux comprendre la physiopathologie de la myopathie à agrégats tubulaires et ainsi pouvoir proposer des solutions thérapeutiques efficaces
Myopathy 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
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Libros sobre el tema "STIM1"

1

Stimm, Thomas. Thomas Stimm: Keramik 1987-2001. Wien: Kunst Bundeskanzleramt, 2002.

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Hanson, Sten. Det praktiska tonsätteriets historia: Föreningen svenska tonsättare genom 75 år. [Stockholm]: Edition Reimers, 1993.

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Predi, Renzo. Metodi di stima delle strutture familiari. Bologna: CLUEB, 1991.

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I metodi di stima nella progettazione. Roma: Gangemi, 1985.

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Heusser, Pierre. Stimm- und Wahlrecht für Ausländerinnen und Ausländer. Zürich: Schulthess, 2001.

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Sonderforschungsbereich 447 "Kulturen des Performativen.", ed. Stimm-Welten: Philosophische, medientheoretische und ästhetische Perspektiven. Bielefeld: Transcript, 2009.

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Amodio, Fabia Peschitz. No, se non hai stima di me--. Pasian di Prato (Udine): Campanotto, 2004.

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Stimm, Oswald. Oswald Stimm: Der Tänzer in der Zeit. Gumpoldskirchen: D.E.A. Verlag, 2016.

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Patent, copyright & trademark / by Richard Stim. Berkeley, CA: Nolo, 2010.

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M, Bonnor G. y Pacific Forestry Centre, eds. A guide to the STIM growth model. Victoria, B.C: Pacific Forestry Centre, 1995.

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Capítulos de libros sobre el tema "STIM1"

1

Jabbari, Parnian y Nima Rezaei. "STIM1 Deficiency". En Genetic Syndromes, 1–4. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-319-66816-1_100-1.

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Frischauf, Irene, Marc Fahrner, Isaac Jardín y Christoph Romanin. "The STIM1: Orai Interaction". En Advances in Experimental Medicine and Biology, 25–46. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-26974-0_2.

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Choi, Seok, Jozsef Maleth, Archana Jha, Kyu Pil Lee, Min Seuk Kim, Insuk So, Malini Ahuja y Shmuel Muallem. "The TRPCs–STIM1–Orai Interaction". En Handbook of Experimental Pharmacology, 1035–54. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-05161-1_13.

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Yee, Christina. "Calcium Channel Defects (STIM1 and ORAI1)". En 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)". En 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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Bodnar, Dora, Woo Young Chung, Dongki Yang, Jeong Hee Hong, Archana Jha y Shmuel Muallem. "STIM-TRP Pathways and Microdomain Organization: Ca2+ Influx Channels: The Orai-STIM1-TRPC Complexes". En Store-Operated Ca²⁺ Entry (SOCE) Pathways, 139–57. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-57732-6_8.

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Woo, Jin Seok, Sonal Srikanth y Yousang Gwack. "Modulation of Orai1 and STIM1 by Cellular Factors". En 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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Wang, Wen-An y Nicolas Demaurex. "Proteins Interacting with STIM1 and Store-Operated Ca2+ Entry". En Cellular Biology of the Endoplasmic Reticulum, 51–97. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-67696-4_4.

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Ng, Lih Chyuan, Judith A. Airey y Joseph R. Hume. "The Contribution of TRPC1 and STIM1 to Capacitative Ca2+ Entry in Pulmonary Artery". En Advances in Experimental Medicine and Biology, 123–35. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60761-500-2_8.

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Zhou, Yandong, Youjun Wang y Donald L. Gill. "Assessing the Molecular Nature of the STIM1/Orai1 Coupling Interface Using FRET Approaches". En 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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Actas de conferencias sobre el tema "STIM1"

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Hubrack, Satanay, Ethel Adap, Stefan Feske y Khaled Machaca. "Role Of Stim1 And Orai1 In Mammalian Oocyte Activation". En 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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Aravamudan, Bharathi, Justin Drawz, Michael A. Thompson, Christina Pabelick, Y. S. Prakash y Gary Sieck. "Inflammation-Induced STIM1 Aggregation In Human Airway Smooth Muscle Cells". En American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a2146.

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Babicheva, A., R. Powers, P. P. Jain, M. Xiong, A. Makino y J. X. J. Yuan. "STIM1 Contributes to Endothelial-to-Mesenchymal Transition in Pulmonary Hypertension". En American Thoracic Society 2024 International Conference, May 17-22, 2024 - San Diego, CA. American Thoracic Society, 2024. http://dx.doi.org/10.1164/ajrccm-conference.2024.209.1_meetingabstracts.a7136.

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Latour, Simon, Isabelle Mahouche, Floriane Cherrier, Jean-Philippe Merlio, Sandrine Poglio y Laurence Bresson Bepoldin. "Abstract 1881: STIM1 and Orai1 control non-Hodgkin lymphoma cells migration". En 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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Yang, Shengyu, Jianwei Sun y Huifang He. "Abstract 4317: Stim1 and Orai1 are critical regulators of melanoma invasion and anoikis". En 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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Li, Yongsheng. "Abstract A198: A novel regulatory circuit involving STIM1 and HIF-1 mediates hypoxia-driven hepatocarcinogenesis". En Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; November 5-9, 2015; Boston, MA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1535-7163.targ-15-a198.

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Li, Yongsheng. "Abstract 5149: A novel regulatory circuit involving STIM1 and HIF-1 mediates hypoxia-driven hepatocarcinogenesis". En Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-5149.

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Umemura, Masanari, Erdene Baljinnyam, Lai-Hua Xie, Stefan Feske, Martha Nowycky y Kosaku Iwatsubo. "Abstract 5259: Role of Orai1 and STIM1 in store-operated Ca2+ entry and cell migration in melanoma". En Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-5259.

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Pradyumna Kulkarni, Rashmi, Nancy Nader, Ethel Alcantara-adap, Maya Dib y Khaled Machaca. "To Be Or Not To Be: Mechanisms Of Regulation Of Stim1 By Its 3'utr In Breast Cancer". En Qatar Foundation Annual Research Conference Proceedings. Hamad bin Khalifa University Press (HBKU Press), 2014. http://dx.doi.org/10.5339/qfarc.2014.hbpp0199.

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Ito, Satoru, Nobukazu Suganuma, Hiromichi Aso, Masashi Kondo, Mitsuo Sato y Yoshinori Hasegawa. "STIM1 Regulates Ca2+ Influx And Migration Induced By Platelet-Derived Growth Factor In Human Airway Smooth Muscle Cells". En American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a3575.

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Informes sobre el tema "STIM1"

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Savard, Annie, Alexandre Cavalcante y Daniela Caprioara. L’enseignement des mathématiques dans les écoles secondaires du Québec: L’alignement entre les enseignants, les concepts mathématiques des programmes ministériels et les concepts mathématiques utilisés dans les emplois STIM. CIRANO, 2022. http://dx.doi.org/10.54932/mldf5092.

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Ce rapport présente une étude portant sur les concepts et processus enseignés à l’école secondaire au Québec. Il étudie l’alignement entre les concepts enseignés et les concepts utilisés par des travailleurs de l’industrie STIM du Québec, l’alignement entre les motivations et les tensions des enseignants et les concepts mathématiques enseignés, ainsi que l’alignement entre l’épistémologie des enseignants de mathématiques du secondaire, les concepts mathématiques du programme de formation et les mathématiques utilisées par les travailleurs de l’industrie STIM. Dans un premier temps, nous avons fait une analyse des concepts et des processus mathématiques présents dans le programme de formation de l’école québécoise du secondaire, volet mathématique. Nous avons comparé cette analyse avec d’autres programmes de mathématiques. Nous avons étudié les métiers STIM représentés dans les manuels scolaires québécois. Dans un deuxième temps, nous avons interrogé des travailleurs STIM quant aux concepts mathématiques employés dans le cadre de leur travail. Nous avons comparé ces concepts mathématiques à ceux présents dans le Programme de formation de l’école québécoise. Dans un troisième temps, nous avons interrogé des enseignants de mathématiques du secondaire quant à leurs représentations des concepts mathématiques du programme. Nous leur avons fait parvenir un questionnaire et nous avons réalisé des groupes de discussion. Nous avons comparé leurs représentations de ces concepts mathématiques à ceux présents dans le Programme de formation de l’école québécoise. Nos résultats suggèrent que certains concepts mathématiques sont beaucoup utilisés par les travailleurs STIM, mais sont peu enseignés au secondaire. C’est le cas des statistiques qui sont principalement enseignées aux élèves du volet Culture Société Technique, volet qui ne conduit pas à se qualifier dans les programmes STIM du cégep et de l’université. Qui plus est, une grande proportion des enseignants rencontrés disent ne pas apprécier les statistiques. Ces résultats montrent un désalignement important qui pourrait conduire les élèves à une vision tronquée des mathématiques utilisées dans les carrières STIM.
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Deutsch-Heng, Mikhael, Benoit Dostie y Geneviève Dufour. Documenter l’évolution de la demande des compétences liée aux STIM. CIRANO, enero de 2022. http://dx.doi.org/10.54932/hajn9336.

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Quel est l’impact des changements technologiques sur la demande de compétences ? Qu’en est-il pour les compétences plus particulièrement liées aux professions STIM ? Pour le déterminer, nous apparions les données occupationnelles des Recensements canadiens de 2006 et 2016 à des données détaillées qui associent à chaque occupation des mesures d'habileté et compétences requises pour occuper ces dernières. Nous trouvons que la demande des compétences liées aux mathématiques a augmenté pendant cette période, mais que l’augmentation est concentrée chez les professions STIM et les professions liées aux STIM. Nous trouvons aussi que les changements dans la demande de compétences s’observent à l’intérieur d’occupations définies finement, plutôt que par des changements dans la structure occupationnelle.
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Belzil, Christian, Jorgen Hansen y Julie Pernaudet. Les déterminants cognitifs et non-cognitifs du choix de filière et leur impact sur la phase initiale du cycle professionnel. CIRANO, mayo de 2024. http://dx.doi.org/10.54932/zmct9599.

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Grâce à la collecte de données nous permettant de relier les trajectoires éducatives des individus à différentes mesures de compétences, nous étudions les déterminants des choix de filières au Québec et dans le reste du Canada et en particulier, le rôle des compétences cognitives et non-cognitives. Nous évaluons l’impact des études en Sciences, Technologie, Ingénierie, et Mathématiques (STIM) ainsi que l’effet des facteurs cognitifs et non-cognitifs sur un grand nombre de mesures de performance sur le marché du travail. Nos résultats indiquent que les performances individuelles dans le test EIACA (semblable au test PISA) n’ont pratiquement aucun pouvoir prédictif sur la probabilité de compléter un programme scientifique mais jouent un rôle déterminant sur les salaires à 30 ans. La fréquentation d’un programme STIM est principalement expliquée par la compétence académique en mathématiques mesurée par les notes obtenues à l'âge de 18 ans. Le second déterminant le plus important est de loin le facteur non-cognitif mesurant le degré de motivation pendant les études. Toutes choses égales par ailleurs (à compétences égales), les Ontariens ont une probabilité d’obtenir un diplôme STIM plus élevée que les Québécois.
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Dufour, Genevieve, Nathalie de Marcellis-Warin y Molivann Panot. Améliorer les compétences en mathématiques au Québec: Cinq recommandations tirées d’En avant math ! CIRANO, febrero de 2023. http://dx.doi.org/10.54932/dlcb6893.

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Le CIRANO et le Centre de recherches mathématiques sont partenaires d’En avant math !, une initiative d’envergure nationale pour promouvoir les mathématiques et accroître la numératie. Depuis trois ans, plusieurs travaux ont permis d'identifier des pistes de solutions afin d'assurer le développement d'une main-d'œuvre hautement qualifiée en mathématiques appliquées et favoriser une meilleure adéquation entre les compétences des personnes et les besoins du marché du travail, particulièrement dans les secteurs des sciences, de la technologie, de l'ingénierie et des mathématiques (STIM). Les auteurs présentent ici les principaux enseignements et recommandations qui se dégagent des travaux de la première phase d’En avant math !.
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Haigh, Susan y Mary Lee Kennedy. Observations on Research Libraries’ Alignment with Institutional STEM Priorities / Observations quant à l’alignement des bibliothèques de recherche sur les priorités institutionnelles en STIM. Association of Research Libraries and Canadian Association of Research Libraries, mayo de 2023. http://dx.doi.org/10.29242/report.stem2023.

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This report published by the Association of Research Libraries (ARL) and the Canadian Association of Research Libraries (CARL) synthesizes the two associations’ joint exploration of the need for, and nature of, alignment of research libraries with their universities’ STEM priorities. The report notes the challenges to be overcome, and provides examples of the ways libraries are already working to strengthen and support STEM at their institutions. The report includes a summary of common themes as well as observations of each institution visited.
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Francesca, Crotta. Docenti di oggi e di domani in Ticino: Stime previsionali del fabbisogno di docenti nelle scuole dell’infanzia, elementari, medie e medie superiori entro il 2022/2023. Scuola universitaria professionale della Svizzera italiana, 2019. http://dx.doi.org/10.33683/ins.19.11232.

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7

Haeck, Catherine, Robert Lacroix y Richard E. Tremblay. S’attaquer à la sous-scolarisation des hommes, sans nuire au succès des femmes. CIRANO, marzo de 2023. http://dx.doi.org/10.54932/tqny8179.

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En matière de scolarisation, d’importants bouleversements se sont produits au cours des dernières décennies au Québec. On a assisté à un rattrapage énorme des femmes sur le plan des études universitaires, et en particulier dans certaines disciplines comme l’éducation, la santé et les sciences sociales et sciences de la vie, mais beaucoup moins dans les STIM. Est-ce un problème ? Pas vraiment. Le problème, et c’est là le secret le mieux gardé, c’est du côté des hommes. Dans LA SOUS-SCOLARISATION DES HOMMES ET LE CHOIX DE PROFESSION DES FEMMES à paraître aux Presses de l’Université de Montréal, les auteurs déboulonnent plusieurs mythes et posent un regard critique, réflexif et largement documenté sur les initiatives visant à influencer les choix de carrière des femmes et braquent plutôt les projecteurs sur les enjeux économiques et sociaux du manque de mixité dans des secteurs clés de l’économie.
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Arias, Karla, David López, Segundo Camino-Mogro, Mariana Weiss, Dylan Walsh, Livia Gouvea y Michelle Carvalho Metanias Hallack. Green Transition and Gender Bias: An Analysis of Renewable Energy Generation Companies in Latin America. Editado por Amanda Beaujon Marin. Inter-American Development Bank, septiembre de 2022. http://dx.doi.org/10.18235/0004461.

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This study analyzes how the energy transition might change gender bias in power-generating industries. To this end, this paper employs a sample of 102 renewable energy generation companies from six countries in Latin America and the Caribbean: Bolivia, Chile, Costa Rica, Panama, Mexico, and Uruguay. The analysis of collected data shows that renewable generation companies with the highest relative efficiency in the labor-capital ratio are those with the highest participation of women. In addition, the results show that renewable companies are incrementing recruitment of women in energy generation. Nevertheless, in the analyzed sample, the participation of women in renewables is still lower than the sectorial average. Moreover, there is no structural change with respect to roles that women occupy, when comparing renewables companies with others generation companies. Considering the companies size, bigger renewables companies (with higher installed generation capacity) tend to hire more women, but those women occupy mostly non-technical positions. In addition, women's participation decreases in positions requiring more technical occupations. Women represent 36% of STEM1 employees, 39% of non-STEM employees, and 48% of non-qualified employees of the renewable generation companies surveyed. Concerning the role of women in decision making roles within energy companies, wide gender gaps exist in executive and management positions; the proportion of females in the boardroom and in management roles for renewables generation companies was 24% and 22%, respectively. Furthermore, 68% of surveyed companies did not have a gender policy in place. This study confirms that a change in technology alone does not generate qualitative changes in the labor market from a gender perspective. Such changes would be achieved by complementing technological change with inclusion policies, encouraging women to study careers related to science and technology to fill the shortage of female professionals in these areas, and closing the knowledge gap through systematic data collection and sharing about gender in the energy workforce.
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