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Lejard, Véronique. "Etude de la régulation transcriptionnelle du collagène de type I dans les fibroblastes tendineux". Paris 6, 2007. http://www.theses.fr/2007PA066465.
Pełny tekst źródłaSolovey, Maria [Verfasser], i Andreas [Akademischer Betreuer] Burchert. "Nuclear factor of activated T-cells, NFATC1, governs FLT3-ITD-driven hematopoietic stem cell transformation and a poor prognosis in AML / Maria Solovey ; Betreuer: Andreas Burchert". Marburg : Philipps-Universität Marburg, 2019. http://d-nb.info/1202110460/34.
Pełny tekst źródłaCatherinet, Claire. "Etude des effecteurs de la voie Ca2+/Calmoduline dans les leucémies aiguës lymphoblastiques T". Thesis, Sorbonne Paris Cité, 2017. http://www.theses.fr/2017USPCC293/document.
Pełny tekst źródłaT cell acute lymphoblastic leukemia (T-ALL) is an aggressive malignancy of T cell progenitors. Despite initial response to chemotherapy, relapses remain frequent in children and adults. Previous results identify sustained activation of Calcineurin (Cn)/NFAT signaling pathway in human T-ALL and murine T-ALL models. Importantly, they also demonstrated Cn is essential for T-ALL Leukemia Initiating Cells (LIC) activity in a murine model of T-ALL induced by an activated allele of NOTCH1 (ICN1). Since pharmacologic inhibition of Cn induces side effects, we aim to identify downstream effectors involved in T-ALL. NFAT (Nuclear Factor of Activated T cells) factors play crucial roles downstream Cn during development and activation of T cells. To address their role in T-ALL, we generated mouse ICN1-induced T-ALL in which NFAT genes can be inactivated either single or in combination following Cre-mediated gene deletion. We demonstrated that (i) NFAT factors are required downstream Cn for LIC activity in T-ALL in vivo (ii) ex vivo NFAT factors deletion alters survival, proliferation and migration of T-ALL (iii) NFAT1, 2 and 4 have a largely redundant function in T-ALL. Moreover, the NFAT-dependant transcriptome allowed to identify important targets (CDKN1A, MAFB) involved in T-ALL survival and proliferation in vitro. Calmodulin-dependant kinases (CaMK) are kinases activated by calcium signaling in T cells. We showed that pharmacologic inhibition of CaMKs in ICN1-induced T-ALL alters survival and proliferation of T-ALL in vitro. Beside, specific inhibition by RNA interference of CaMKIIg and CaMKIId suggests a putative role of these kinases in T-ALL maintenance
Arabanian, Laleh Sadat. "Role of NFAT (Nuclear Factor of Activated T Cells) Transcription Factors in Hematopoiesis". Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2012. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-99739.
Pełny tekst źródłaUlrich, Jason Daniel. "The regulaton and function of nuclear factor of activated T-cells in neurons". Diss., University of Iowa, 2011. https://ir.uiowa.edu/etd/2782.
Pełny tekst źródłaArabanian, Laleh Sadat [Verfasser], Gerhard [Akademischer Betreuer] Rödel, Alexander [Akademischer Betreuer] Kiani i Gerhard [Akademischer Betreuer] Ehninger. "Role of NFAT (Nuclear Factor of Activated T Cells) Transcription Factors in Hematopoiesis / Laleh Sadat Arabanian. Gutachter: Gerhard Rödel ; Alexander Kiani ; Gerhard Ehninger. Betreuer: Gerhard Rödel". Dresden : Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2012. http://d-nb.info/1068148918/34.
Pełny tekst źródłaBaggott, Rhiannon Rebecca. "Role of the plasma membrane calcium ATPase as a negative regulator of angiogenesis". Thesis, University of Wolverhampton, 2014. http://hdl.handle.net/2436/332139.
Pełny tekst źródłaZhang, Danfeng [Verfasser], i Benito A. [Akademischer Betreuer] Yard. "The role of nuclear factor of activated T cells 5 (NFAT5) in inflammation and the potential use of bifunctional enzyme triggered carbon monoxide releasing molecule in treatment of systemic inflammation / Danfeng Zhang ; Betreuer: Benito Yard". Heidelberg : Universitätsbibliothek Heidelberg, 2020. http://nbn-resolving.de/urn:nbn:de:bsz:16-heidok-279386.
Pełny tekst źródłaZhang, Danfeng [Verfasser], i Benito [Akademischer Betreuer] Yard. "The role of nuclear factor of activated T cells 5 (NFAT5) in inflammation and the potential use of bifunctional enzyme triggered carbon monoxide releasing molecule in treatment of systemic inflammation / Danfeng Zhang ; Betreuer: Benito Yard". Heidelberg : Universitätsbibliothek Heidelberg, 2020. http://d-nb.info/1205807497/34.
Pełny tekst źródłaChebel, Amel. "Influence de la stimulation et de la sénescence réplicative des lymphocytes T sur le métabolisme des télomères". Thesis, Lyon 1, 2010. http://www.theses.fr/2010LYO10008.
Pełny tekst źródłaLymphocytes are an example of somatic cells capable to induce telomerase activity when stimulated. We showed that lymphocytes, during long-term culture and repeated PHA stimulations, present a progressive drop in telomerase activity interrupted at each stimulation by a transitory increase. These variations are positively correlated with hTERT and telomere length variations. γ-H2AX and 53BP1 foci and their localization on telomeres increase with cell aging. We show a telomere dysfunction during in vitro lymphocyte senescence resulting from an excessive telomere shortening and a decrease in shelterin content. The mechanism involved in early variations of hTERT expression during lymphocyte activation remained to be understood. Consequences of lymphocyte treatment with different immunosuppressors, all acting directly or indirectly on NFAT activation, suggested a role for NFAT in the regulation of hTERT transcription. Five putative responsive elements for NFAT were identified in the hTERT promoter. We showed that NFAT activates in vitro the hTERT promoter mainly via a consensus site localized in the promoter core at position -40 and a functional synergy between NFAT and SP1. Furthermore, NFAT1 binds directly to the endogenous hTERT promoter via this consensus site in vivo. Thus, NFAT positively regulates the hTERT transcription and we propose its implication in telomerase activation during lymphocyte stimulation
Houlard, Martin. "Étude de l'adressage et de l'implication nucléaire du proto-oncogène Vav-1". Paris 7, 2002. http://www.theses.fr/2002PA077098.
Pełny tekst źródłaHabas, Agata M. "The role of Nuclear Factors of Activated T-cells (NFAT) in neuronal death". 2004. http://etd.louisville.edu/data/UofL0109t2004.pdf.
Pełny tekst źródłaLo, Yu-Hsun, i 駱育壎. "The role of promyelocytic leukemia ( PML) protein in transcriptional activation of nuclear factor of activated T cell". Thesis, 2008. http://ndltd.ncl.edu.tw/handle/02681520577581507177.
Pełny tekst źródła國立陽明大學
微生物及免疫學研究所
96
Abstract The promyelocytic leukemia protein (PML) is a tumor suppressor. It is involved in many different physiological functions but the complicated action mechanisms are not yet fully understood. PML localizes in the nucleus to form speckles called PML nuclear bodies, containing regulatory proteins, such as p53, Daxx, CREB binding protein (CBP) and small ubiquitin-related modifier(SUMO-1). Nuclear factor of activated T cell (NFAT) is an important transcription factor, regulates many key T cell functions. In this study, we found that NFAT is an unexpected partner of PML: PML specifically enhanced the transcription activation of NFAT in T cells and 293 cells. In PML-null mouse embryonic fibroblasts, no transcription activity of NFAT could be detected, while PML expression restored NFAT activation. In constrast, PML was not regulated for NF-�羠 transcription. Sumoylation of PML was essential for PML to promote the transcription activity of NFAT. The additive effect of PML was not due to sequestration of Daxx by PML. There was a selective requirement of PML isoform in NFAT activation. PML-I and PML-VI, but not PML-IV, enhanced NFAT transactivation. The potential interaction between NFAT and PML was demonstrated by co-immunoprecipitation of NFATc with PML-I, PML-IV, or PML-VI. GST pull down assay further illustrated a direct binding between the NFAT-homology region (NHR) of NFATc and the RING finger, B-boxes of PML. Inside nucleus of activated T cells, NFATc was found co-localized with PML speckles. Even though PML overexpression did not increase nuclear localization of NFATc, knockdown of PML was moderately reduced nuclear presence of NFAT. Some, but not all, of NFAT activity-mediated genes expression were regulated by PML. The interaction of PML with NFATc in vivo was further confirmed by chromatin immunoprecipitation (ChIP) and DNA affinity precipitation assay (DAPA) analysis. Knockdown of PML was also associated with reduced promoter binding of NFAT and CBP. It is suggested that part of mechanisms of underlying enhancement of NFATc transactivation mediated by PML is due to stabilization of NFAT-CBP transcriptional complex. The unexpected coupling of PML with NFAT reveals a novel mechanism underlying the diverse physiological functions of PML.
Chow, Winsion. "The role of nuclear factor of activated T-cells-c1 in the vascular smooth muscle cell response to injury". 2007. http://link.library.utoronto.ca/eir/EIRdetail.cfm?Resources__ID=789015&T=F.
Pełny tekst źródłaLin, Chih-Chung, i 林志忠. "Investigation on the Calcineurin-Nuclear Factor of Activated T-Cell Signal Transduction Pathway in a Porcine Model of Atrial Fibrillation". Thesis, 2003. http://ndltd.ncl.edu.tw/handle/75264169965673901035.
Pełny tekst źródła國立臺灣大學
藥理學研究所
91
Background Cytosolic calcium overloading occurs in atrial fibrillation tissue. We therefore investigated the calcium-activated calcineurin-nuclear factor of activated T-cell (NFAT) pathway in atrial tissue in a porcine model of atrial fibrillation. Methods and Results Atrial fibrillation was induced in adult pigs by rapid atrial pacing at a rate of 600 per minute. Atrial tissue from the left atrium was obtained 6 weeks after implantation of the pacemaker (pacing for 4 weeks and atrial fibrillation without pacing for 2 weeks). We found that calcineurin enzyme activity increased significantly in pigs with atrial fibrillation when compared to control pigs (0.143OD620 ± 0.013 vs 0.038OD620 ± 0.028, p < 0.01). We found that both NFATc3 and NFATc4, the down stream effectors of calcineurin, increased significantly in the nuclei in atrial fibrillation tissue using immunoblotting. Translocation of NFATc3 and NFATc4 into the nuclei was also demonstrated in atrial tissue microsections using immunohistochemistry. The electrophoretic mobility shift assay further demonstrated that nuclear extracts from atrial fibrillation tissue had a significantly larger binding capacity for NFAT specific oligonucleotide probes. Conclusion Our results demonstrated that calcineurin activity was increased in atrial fibrillation tissue with subsequent NFATc3 and NFATc4 translocation into the nucleus. Activation of this signal transduction pathway may play an important role in the pathogenesis of atrial fibrillation.