Thèses sur le sujet « Inversion de la mort cellulaire »
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Lagorgette, Lisa. « Rôle de la phosphatase Wip1 dans la nécroptose ». Electronic Thesis or Diss., Bourgogne Franche-Comté, 2024. http://www.theses.fr/2024UBFCI008.
Texte intégralPhosphorylation of critical proteins in cell death pathways is well described in the literature, but mostly from the point of kinases. Dephosphorylation is usually studied much less, but phosphatases could prevent the execution of suicidal cell death programs. Necroptosis appears as a new type of programmed cell death knows for its immunogenic properties. Inducing immunogenic cell death could be proposed to improve cancer treatment and avoid multidrug resistance. Overexpressed in several cancers, the phosphatase PPM1D, also named Wip1, is described as central regulator of cell death pathways such as apoptosis, autophagy or senescence. This work investigates the role of the phosphatase Wip1 in the programmed necroptosis cell death. Using several genetically deficient cell line models, we propose Wip1 as a negative regulator of necroptosis through its interaction with the kinase RIP3 into the nucleus. Finally, Wip1 inhibition is proposed as a promising therapeutic strategy in order to improve immunogenic cell death induction
DEPRAETERE, VALERIE. « Recherche de molecules signalisatrices de la mort cellulaire developpementale et de la mort cellulaire induite par irradiation ». Aix-Marseille 2, 1999. http://www.theses.fr/1999AIX22016.
Texte intégralFERNANDEZ, PIERRE-ALAIN. « Analyse cellulaire et moleculaire de la mort cellulaire programmee des vertebres ». Paris 6, 1995. http://www.theses.fr/1995PA066321.
Texte intégralCornillon, Sophie. « Etudes preliminaires sur la mort cellulaire chez dictyostelium ». Aix-Marseille 2, 1998. http://www.theses.fr/1998AIX22011.
Texte intégralRaoul, Cédric. « Mort développementale et pathologique du motoneurone spinal : Implication du récepteur de mort Fas (CD95) ». Aix-Marseille 2, 2002. http://www.theses.fr/2002AIX22018.
Texte intégralChimienti, Fabrice. « Regulation du zinc cellulaire : consequences sur la mort programmee ». Paris 5, 2001. http://www.theses.fr/2001PA05S002.
Texte intégralGaumer, Sébastien. « Etude de bcl-2 dans la mort cellulaire programmée ». Versailles-St Quentin en Yvelines, 2001. http://www.theses.fr/2001VERS0004.
Texte intégralMoustapha, Aoula. « Etude mécanistique de la mort cellulaire induite par la curcumine dans un modèle cellulaire d’hépatocarcinome ». Paris 6, 2013. http://www.theses.fr/2013PA066466.
Texte intégralCurcumin, a major active component of turmeric Curcuma longa, L. , has been shown to have inhibitory effects on cancers. In vitro studies suggest that curcumin inhibits cancer cell growth by activating apoptosis, but the mechanisms underlying the anticancer effects of curcumin are unclear. We have dissected the mechanistic consequences of endoplasmic reticulum (ER) and lysosomal destabilization involved in a mitochondrially associated apoptosis. Curcumin at 25 M induces an ER stress with calcium release which, in turn, destabilizes the mitochondrial compartment to induce apoptosis. These events are also associated with lysosomal membrane permeabilization and activation of caspase-8 mediated by activation of cathepsins and calpains which induce Bid cleavage. Recently, it has been suggested that enhanced autophagy may play an important role in cancer therapy. In this work, I show that a fine interplay is at work which involves early autophagy as soon as the mitochondria produce superoxide anions and hydrogen peroxide. Induction of autophagy, as shown by autophagic vacuole formation, was detected by acridine orange staining and monodansylcadaverine dye after exposure to curcumin at a concentration of 25 M at which only early events of apoptosis are detectable. Conversion of LC3-I to LC3-II, a marker of active autophagosome formation, was also detectable by Western blotting following curcumin treatment. We also observed that reactive oxygen species production and autophagic vacuole formation following curcumin treatment was almost completely blocked by N-acetylcystein or by the mitochondrial specific antioxidant MitoQ, but also by the mitochondrial calcium uniporter inhibitor ruthenium red and to a lesser extend by the calcium chelators, BAPTA-AM and EGTA-AM. Curcumin-induced autophagy failed to rescue the cell from death and the cells undergo apoptosis after a try for survival. Curcumin successfully induces oxidative stress in Huh-7 cells, perturbs important cell survival mechanisms, and thus achieves high degree of killing of these cancer cells
Morel, Jean-Benoît. « Analyse genetique et moleculaire de la mort cellulaire et de suppresseurs de la mort cellulaire en relation avec la reponse hypersensible chez arabidopsis thaliana ». Paris 11, 1998. http://www.theses.fr/1998PA112236.
Texte intégralDUNEAU, Mélanie. « GALIG : UN NOUVEAU GÈNE HUMAIN INDUCTEUR DE LA MORT CELLULAIRE ». Phd thesis, Université d'Orléans, 2005. http://tel.archives-ouvertes.fr/tel-00010769.
Texte intégralSt-Michel, Chantale. « Les régulateurs de la mort cellulaire programmée chez les végétaux ». Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape7/PQDD_0007/MQ44964.pdf.
Texte intégralGoéré, Diane. « Caractérisation de la mort cellulaire induite par un anticorps trifonctionnel ». Phd thesis, Université Paris Sud - Paris XI, 2013. http://tel.archives-ouvertes.fr/tel-00870033.
Texte intégralMoreira, Wilfried. « Stress oxydatif, différentiation et mort cellulaire chez le parasite Leishmania ». Thesis, Université Laval, 2011. http://www.theses.ulaval.ca/2011/28186/28186.pdf.
Texte intégralGoere, Diane. « Caractérisation de la mort cellulaire induite par un anticorps trifonctionnel ». Thesis, Paris 11, 2013. http://www.theses.fr/2013PA11T022/document.
Texte intégralThe development of cancer in an immunocompetent individual reflects, in part, a tumor escape from the immunosurveillance. The tumor escape is a complex, multifactorial, in which tumor cells will evade the defense mechanisms of the host by changing their microenvironment. Therefore, restoration or induction of these defense mechanisms is one of the therapeutic strategies against cancer. One of the principles of immunotherapy is based on the injection of antibodies that target tumor cells or effector cells of immunity. The anti-tumor efficacy of these antibodies has been greatly improved by a better understanding of modes of action and modulatory effects of these antibodies.Thus, to optimize the action of immune effectors to tumor cells, a bispecific antibody, trifunctional: catumaxomab, capable of binding to the adhesion molecule of the epithelial cells (EpCAM), expressed by tumor cells and the CD3 antigen of T cells, has been developed mainly in intraperitoneal treatment of refractory malignant ascites.The objective of this study was to determine the immunomodulatory effects of catumaxomab on tumoral cells expressing EpCAM, from two experimental models (allogeneic and autologous), evaluate and characterize cytotoxicity induced by catumaxomab, and analyze the presence of stress signals inducing immunogenic cell death such as membrane exposure of calreticulin by pre-apoptotic tumor cells, release of HMGB1 and of adenosine triphosphate (ATP) in the extracellular medium, inducing a T cell activation.In the presence of EpCAM + cells, catumaxomab induced a major the activation of T cells (expression of CD69, CD107a, HLA-DR and PD1), stimulated an inflammatory response Thelper type 1 (Th1) and the synthesis of interferon-gamma by CD8 T cells. Catumaxomab committed CD16 NK cells and monocytes. More, in models allogeneic catumaxomab, caused cell death associated with ATP release and induced an immunogenic cell death after pre-incubation of oxaliplatin.Therefore, catumaxomab modulates the immune environment in malignant ascites, and convert chronic and immunosuppressive inflammation (Th2) in acute and immunogenic inflammation (Th1). However, in these conditions, catumaxomab alone does not seem to trigger immunogenic cell death.the cytotoxicity of this bispecific antibody could be enhance by different techniques: (1) combining with chemotherapy such as oxaliplatin to promote immunogenic cell death, (2) refining its action on CD3 lymphocytes by changing its spatial configuration (BiTE antibody), (3) increasing its affinity for the FcR of accessory cells (Fc aglycosylated), (4) increasing its cytotoxicity by changing the target directed against the immune molecule (anti-PD-1 ...). Finally, the clinical use could be facilitated by this humanizing murine chimeric antibody to prevent the formation of anti-murine antibodies directed against catumaxomab.A phase II clinical trial aimed to evaluate the efficacy of intraperitoneal catumaxomab after complete cytoreductive surgery of gastric carcinomatosis in patients who received preoperative systemic chemotherapy with oxaliplatin have just started. In this study, we will validate the ability of catumaxomab 1) to induce immunogenic cell stress and death of cancer cells, 2) to change the polarization of effector cells to Th1 inflammatory disease, 3) to promote the expression of costimulatory molecules and TRAIL on NK cells and monocytes, and we will correlate these immune biomarkers to treatment efficacy
Tresse, Emilie. « Etude génétique de la mort cellulaire autophagique chez Dictyostelium discoideum ». Aix-Marseille 2, 2008. http://theses.univ-amu.fr.lama.univ-amu.fr/2008AIX22113.pdf.
Texte intégralAutophagic cell death is still incompletely defined despite its pathophysiological importance, notably during cancers and neurodegenerative diseases. In the protist Dictyostelium discoideum, autophagic cell death is induced during development. In this model organism, autophagic cell death proceeds in two steps, first, a sensitization step induced by starvation and leading to autophagy, and then an induction step by the physiological morphogen DIF-1, leading to cell death proper. To identify molecules implicated in this autophagic cell death, we used a random mutagenesis strategy. This strategy allowed us to obtain two cell death mutants. The first mutant led us to explore the role of glucose homopolymers during autophagic cell death. Our results demonstrate that a UDP-glucose derivative is necessary for autophagic cell death and that the metabolic state of cells during the sensitization stage predetermines the signalisation pathways used for cell death induction. The second mutant led us to demonstrate the role of talin, a scaffoldi protein implicated in cytoskeleton dynamics, during signalisation of cell death induction. This strategy of random insertional mutagenesis is thus a powerful tool allowing description of pathways leading to autophagic cell death. The present work contributes to the molecular definition of this cell death
Duneau, Mélanie. « Galig : un nouveau gène humain inducteur de la mort cellulaire ». Orléans, 2005. http://www.theses.fr/2005ORLE2008.
Texte intégralZhou, Heng. « Mode d'action des composés induits Lytix sur la mort cellulaire ». Thesis, Université Paris-Saclay (ComUE), 2017. http://www.theses.fr/2017SACLS134.
Texte intégralThe oncolytic peptide LTX-315 has been developed as an amphipathic cationic peptide that kills cancer cells and turned out to stimulate anticancer immune responses when locally injected into tumors established in immunocompetent mice. We investigated whether LTX-315 induces apoptosis or necrosis. Transmission electron microscopy or morphometric analysis of chromatin-stained tumor cells revealed that LTX-315 failed to induce apoptotic nuclear condensation and rather induced a necrotic phenotype. Accordingly, LTX-315 failed to stimulate the activation of caspase-3. Moreover, inhibition of caspases by Z-VAD-fmk was unable to reduce cell killing by LTX-315. In addition, two prominent inhibitors of necroptosis, necrostatin-1 and cyclosporin A, failed to reduce LTX-315-induced cell death. In conclusion, it appears that LTX-315 triggers unregulated necrosis, which may contribute to its pro-inflammatory and pro-immune effects. Subsequently, we investigated the putative involvement of mitochondria in the cytotoxic action of LTX-315. Subcellular fractionation of LTX-315-treated cells, followed by mass spectrometric quantification, revealed that the agent was enriched in mitochondria. LTX-315 caused an immediate arrest of mitochondrial respiration without any major uncoupling effect. Accordingly, LTX-315 disrupted the mitochondrial network, dissipated the mitochondrial inner transmembrane potential, and caused the release of mitochondrial intermembrane proteins into the cytosol. LTX-315 was relatively inefficient in stimulating mitophagy. Cells lacking the two pro-apoptotic multidomain proteins BAX and BAK, were less susceptible to LTX-315-mediated killing. Moreover, cells engineered to lose their mitochondria were relatively resistant against LTX-315, underscoring the importance of this organelle for LTX-315-mediated cytotoxicity. Altogether, these results support the notion that LTX-315 kills cancer cells by virtue of its capacity to permeabilize mitochondrial membranes. Following, we investigated whether LTX-315 may elicit the hallmarks of immunogenic cell death (ICD). Overally, we observed that LTX-315 induces all known ICD characteristics. This conclusion was validated by several independent methods including immunofluorescence staining, bioluminescence assays, immunoassays, and RT-PCRs. The injection of LTX-315 into established cancers resulted in transiently hemorrhagic focal necrosis that was accompanied by massive release of HMGB1, as well as caspase-3 activation in a fraction of the cells. LTX-315 was equal or more efficient as the positive control, the anthracycline mitoxantrone (MTX), in inducing local inflammation with infiltration by myeloid cells and T lymphocytes. Collectively, these results support the idea that LTX-315 can induce ICD, explaining its capacity to mediate immune-dependent therapeutic effects. The second Lytix compound investigated, LTX-401, is an oncolytic amino acid derivative with potential immunogenic properties. We demonstrated that LTX-401 selectively destroys the structure of the Golgi apparatus. Subcellular fractionation followed by mass spectrometric detection revealed that LTX-401 was selectively enriched in the Golgi rather than in the mitochondria or in the cytosol. The Golgi-dissociating agent Brefeldin A (BFA) reduced cell killing by LTX-401 as it partially inhibited LTX-401-induced mitochondrial release of cytochrome c and the activation of BAX. The cytotoxic effect of LTX-401 was attenuated by the double knockout of BAX and BAK, as well as the mitophagy-enforced depletion of mitochondria, yet was refractory to caspase inhibition. LTX-401 induced all major hallmarks of immunogenic cell death. Moreover, LTX-401-treated tumors manifested a strong lymphoid infiltration. Altogether, these results support the contention that LTX-401 can stimulate immunogenic cell death through a pathway in which Golgi-localized LTX-401 operates upstream of mitochondrial membrane permeabilization
Oizel, Kristell. « Métabolisme et sensibilité à la mort cellulaire dans le glioblastome ». Nantes, 2015. https://archive.bu.univ-nantes.fr/pollux/show/show?id=a1401556-8497-464e-bdda-d0068fe3297e.
Texte intégralTumor cells undergo metabolic adaptations allowing them to sustain a high proliferative rate and to resist to cell death signals, especially increasing aerobic glycolysis and glutaminolysis. Glioblastoma multiforme (GBM), the most common brain tumor in adults, is characterized by a strong resistance to therapeutic treatments and the presence of cancer stem cells. This PhD project investigated the link between metabolism and cell death sensitivity in GBM. First, we studied the impact of isocitrate dehydrogenase (IDH) mutation recently identified in GBM patients. We show that mutated IDH induces a reduced sensitivity to etoposide-induced cell death mediated through a mitochondrial NADH pool reduction. Second, we aimed to determine if glutaminolysis inhibition could modulate cell death response in GBM tumor model. We show that epigallocatechin gallate (EGCG), an inhibitor of glutamate dehydrogenase (GDH), can sensitize GBM cell lines to cell death. Furthermore, in primary cultures models, EGCG sensitize the GBM mesenchymal subtype to cell death. This cellular model derived directly from patients tumors allows to keep the initial tumor heterogeneity, in particular the presence of cancer stem cells. These results show a direct link between metabolism and cell death resistance and open new therapeutic strategies. Thus EGCG could be a good candidate as an adjuvant in current GBM therapy in the context of personalized treatment
Arshad, Muhammad Imran. « Role of IL-33/ST2 axis in acute hepatitis ». Rennes 1, 2012. http://www.theses.fr/2012REN1B103.
Texte intégralInterleukin-33 (IL-33), an alarmin cytokine of IL-1 family, is primarily expressed by endothelial cells and epithelial cells in various inflammatory pathologies in mice and human. IL-33 mediates its biological activity by interaction with specific ST2 and IL-1RAcP receptors. The novel cellular sources of IL-33 and its regulation particularly in liver remain obscure. The objective of my thesis was to better determine the expression, regulation and functions of IL-33 as an alarmin during murine acute hepatitis induced by CCl4, ConA, FasL/Jo2, D-GalN-TNF-α, Poly(I:C) and MHV3 as well as in human patients suffering from HBV fulminant hepatitis. IL-33 was over-expressed in all studied murine hepatic models with induced expression in liver sinusoidal endothelial cells and vascular endothelial cells. The IL-33 over-expression associated with hypervascularisation was also found in HBV fulminant hepatic patients. More surprisingly, we found that IL-33 was expressed in hepatocytes during ConA, Poly(I:C) and MHV3 mediated acute hepatitis in mice. We demonstrated that NKT cells and cell death inducing molecule TRAIL regulated the hepatocyte-specific IL-33 expression during ConA-hepatitis. The PARP-1-RIPK1-RIPK3 mediated necroptosis (or programmed necrosis) in ConA liver injury regulated IL-33 expression in hepatocytes. This leads to the concept of IL-33 as a marker of necroptosis. At functional level, IL-33 had a protective impact in ConA-induced liver injury supporting the current protective role of IL-33/ST2 axis in liver pathology. In conclusion, we evidence a novel NKT cells, TRAIL, PARP-1 and RIP kinases dependent regulatory mechanism for IL-33 in liver pathophysiology. These findings suggest an important role of IL-33/ST2 axis in liver diseases
Villa, Elodie. « Échapper à la mort cellulaire dans le cancer : mitophagie et régulation de la mort indépendante des caspases ». Electronic Thesis or Diss., Université Côte d'Azur (ComUE), 2017. http://www.theses.fr/2017AZUR4109.
Texte intégralOne of the hallmarks of tumor cells is their ability to escape cell death.To achieve this, they have developed a strategy of selectively removing damaged mitochondria by a process of mitophagy. The main actor of mitophagy is the ubiquitin ligase Parkin; but it is mutated or absent in the majority of cancers. We have discovered that another ligase, ARIH1, belonging to the same family of RBR ligases as Parkin, is capable of inducing mitophagy in response to stress. In contrast to Parkin, ARIH1 is overexpressed in many cancers, especially in lung cancer, allowing an increase in mitophagy conferring resistance to stress induced by chemotherapeutic agents. The most characterized cell death pathway is apoptosis, which is directly related to caspases activation. However, it has been established, that caspase inhibition does not prevent cell death because there is another type of cell death called "caspase-independent cell death" or CICD. However, its precise molecular definition is still unknown. Thus for this purpose, pan-genomic siRNA screening was performed and revealed the importance of the ubiquitin / proteasome pathway. In particular, we have been able to identify an enzyme E3 ligase as being protective towards CICD. This enzyme is overexpressed in many cancers and could allow cancer cells to resist CICD and promote tumor progression. In summary, this work has highlighted the importance of ubiquitin ligases in the escape mechanisms to cell death implemented by cancer cells
Villa, Elodie. « Échapper à la mort cellulaire dans le cancer : mitophagie et régulation de la mort indépendante des caspases ». Thesis, Université Côte d'Azur (ComUE), 2017. http://www.theses.fr/2017AZUR4109.
Texte intégralOne of the hallmarks of tumor cells is their ability to escape cell death.To achieve this, they have developed a strategy of selectively removing damaged mitochondria by a process of mitophagy. The main actor of mitophagy is the ubiquitin ligase Parkin; but it is mutated or absent in the majority of cancers. We have discovered that another ligase, ARIH1, belonging to the same family of RBR ligases as Parkin, is capable of inducing mitophagy in response to stress. In contrast to Parkin, ARIH1 is overexpressed in many cancers, especially in lung cancer, allowing an increase in mitophagy conferring resistance to stress induced by chemotherapeutic agents. The most characterized cell death pathway is apoptosis, which is directly related to caspases activation. However, it has been established, that caspase inhibition does not prevent cell death because there is another type of cell death called "caspase-independent cell death" or CICD. However, its precise molecular definition is still unknown. Thus for this purpose, pan-genomic siRNA screening was performed and revealed the importance of the ubiquitin / proteasome pathway. In particular, we have been able to identify an enzyme E3 ligase as being protective towards CICD. This enzyme is overexpressed in many cancers and could allow cancer cells to resist CICD and promote tumor progression. In summary, this work has highlighted the importance of ubiquitin ligases in the escape mechanisms to cell death implemented by cancer cells
Larmonier, Nicolas. « Mort des cellules cancereuses et réponse immunitaire antitumorale ». Dijon, 2004. http://www.theses.fr/2004DIJOMU01.
Texte intégralDrian, Marie-Jeanne. « Effets des agonistes et antagonistes des récepteurs ionotropiques du glutamate sur la survie et la différenciation des cellules néopalliales de rat en culture ». Paris, EPHE, 2000. http://www.theses.fr/2000EPHE3038.
Texte intégralSouissi, Inès. « Etude de l’efficacité d’oligonucléotides leurres de STAT3 dans des cellules tumorales : Analyse de la spécificité et élaboration de séquences discriminantes ». Paris 13, 2012. http://www.theses.fr/2012PA132001.
Texte intégralSTAT3 is a transcription factor of the STAT « Signal Transducer and Activator of Transcription » family. Triggering of cytokine receptors, such as IL-6, activates kinases of the JAK family and results in phosphorylation and dimerization of STAT3. The dimerized STAT3 penetrates the nucleus, binds its targets and activates their transcription. STAT3 is frequently activated in tumor cells; its inhibition generally leads to the death of these cells. STAT1 is another STAT family member; its activation is most of the time linked with cell death or resistance to pathogens. Intriguingly, STAT1 and STAT3, through their DNA Binding Domain (DBD) interact with very similar DNA sequences. In order to achieve specific inhibition of STAT3, hairpin decoy oligodeoxynucleotide sequences (hpdODN) were used. Transfection of the hpdODNs resulted in cell death in the colon carcinoma cell line SW480, demonstrating the efficiency of targeting STAT3's DBD. However, STAT1-dependent Interferon y-induced cell death was blocked by the hpdODN in these cells, suggesting a lack of specificity. Analysis of the mechanism of action of the hpdODN showed that its interaction with activated dimeric STAT3 takes place in the cytoplasm. We further demonstrated that binding of the hpdODN to dimeric STAT3 prevented the binding of importin thereby impairing importin-mediated transport through the nuclear pore. Finally, STAT3 hpdODN complexed with magnetic nanoparticles was tested and found to improve penetration of the hpdODN. An hpdODN inhibiting STATS was tested and found to induce death of hematologic tumor cells with activated STAT5. To further investigate and improve the hpdODN's specificity, comparative 3D analysis of the STAT3 and STAT1 DBDs was conducted. Modifications in the hpdODN sequence were subsequently tested in the SW480 cell line. The new hpdODN induced cell death without preventing interferon y-induced cell death, indicating that the DBD can be used as a basis for specific inhibitory reagents
Aymeric, Laetitia. « Immunogénicite de la mort cellulaire induite par les chimiothérapies anti-cancéreuses ». Phd thesis, Université Paris Sud - Paris XI, 2011. http://tel.archives-ouvertes.fr/tel-00634183.
Texte intégralBruggeman, Quentin. « Caractérisation de suppresseurs de la mort cellulaire programmée chez Arabidopsis thaliana ». Thesis, Paris 11, 2014. http://www.theses.fr/2014PA112317/document.
Texte intégralProgrammed cell death (PCD) is essential for several aspects of plant life, including development and stress responses. Mutational analyses have identified several key PCD components in Arabidopsis thaliana, as the enzyme MIPS1 catalysing the limiting step of myo-inositol (MI) synthesis, crucial cellular compound at the root of many derivatives. One of the most striking features of mips1, disrupted for this protein, is the light-dependent formation of lesions on leaves due to Salicylic Acid (SA)-dependent PCD, revealing roles for MI or inositol derivatives in the regulation of PCD. My thesis work was to find and characterize suppressor of mips1 mutant using two complementary approaches: a gene candidate approach by transcriptomic comparisons and a strategy of direct genetic by screening for extra genic secondary mutations that abolish mips1 cell death phenotype. Analysis of different suppressors revealed the involvement of several factors in MCP, such as the polyadenylation factor CPSF30, a hexokinase or the protein PCB2 operating in chlorophyll biosynthesis. Characterization of these suppressors allowed us to demonstrate crucial role of functions as mRNA maturation, primary carbohydrate metabolism or chloroplastic activity in the regulation of MCP depending on MI accumulation. This work brings many opportunities, to better understand the different regulatory pathways of PCD essential for proper development and to cope with biotic and abiotic stress in plants
Menger, Laurie Colombe Aude. « Effets anticancereux des glucosides cardiotoniques par induction d'une mort cellulaire immunogène ». Phd thesis, Université Paris Sud - Paris XI, 2012. http://tel.archives-ouvertes.fr/tel-00757180.
Texte intégralDjoumad, Abdelmajid. « Crible de mutants de la mort cellulaire programmée chez Arabidopsis thaliana ». Thèse, Université de Sherbrooke, 2010. http://savoirs.usherbrooke.ca/handle/11143/5125.
Texte intégralApetoh, Lionel. « Immunogénicité de la mort cellulaire tumorale provoquée par les thérapies anticancéreuses ». Paris 11, 2008. http://www.theses.fr/2008PA11T015.
Texte intégralDessauge, Frédéric. « Etude des mécanismes de mort cellulaire programmée dans les cellules transformées ». Paris 7, 2004. http://www.theses.fr/2004PA077052.
Texte intégralBarthélémy, Catherine. « Régulation de la mort cellulaire induite par Fas dans les motoneurones ». Aix-Marseille 2, 2004. http://www.theses.fr/2004AIX22036.
Texte intégralLadjimi, Mohamed Tahar. « Modélisation biophysique de la mort cellulaire en réponse au stress thermique ». Thesis, Lille 1, 2019. http://www.theses.fr/2019LIL1R029/document.
Texte intégralThe living cell is constantly exposed to various types of stress that can damage its components. When the induced damages are detected, defense mechanisms are activated to repair them while optimally managing the energy resources available and necessary for cell function. If the stress is too severe and the system can not defend itself, death will be inevitable. The cellular response to stress is orchestrated by intracellular signaling networks that are extraordinarily complex. The molecular species constituting these networks perform various tasks through biochemical reactions, forming synchronized biological process machineries. Our approach in this thesis for the study of these networks is to model them mathematically to reproduce an observed phenomenon and identify its key players, analyze their reactions in response to different signals, and possibly make precise enough and experimentally verifiable predictions that can be of an extreme utility for therapeutic applications. In our studies, we focus on thermal stress and on the resulting cellular response in terms of the dynamics of the molecular species involved, but also of cell fate (death or survival) at the end of the exposure, we adress those questions by dynamic models describing the biochemical kinetics of system variables as a consequence of temperature variation. In a first step, we demonstrate through simulations, followed by experimental validation, that the temporal form of heat stress significantly impacts cell survival. This first result highlights a mechanism of saturation of the repair species as a consequence of exposure to high temperatures. In a second step, we study the potential correlation between a variability introduced on the levels of two proteins in the heat shock response network and the phenomenon of fractional killing. According to our model predictions, experimentally measured chaperone proteins (repair species) variability alone is not sufficient to explain fractional killing, which must involve other sources of variability. Finally, an analysis of the isoeffect curves generated by a generic model of the cellular response to transient stress shows the existence of four sensitivity regimes depending on the duration-intensity parameters of the stress as well as on the parameters of the response network and its time scales. Our work highlights the potential and utility of dynamic network models in the characterization of dose-response curves
Ladjimi, Mohamed Tahar. « Modélisation biophysique de la mort cellulaire en réponse au stress thermique ». Electronic Thesis or Diss., Université de Lille (2018-2021), 2019. http://www.theses.fr/2019LILUR029.
Texte intégralThe living cell is constantly exposed to various types of stress that can damage its components. When the induced damages are detected, defense mechanisms are activated to repair them while optimally managing the energy resources available and necessary for cell function. If the stress is too severe and the system can not defend itself, death will be inevitable. The cellular response to stress is orchestrated by intracellular signaling networks that are extraordinarily complex. The molecular species constituting these networks perform various tasks through biochemical reactions, forming synchronized biological process machineries. Our approach in this thesis for the study of these networks is to model them mathematically to reproduce an observed phenomenon and identify its key players, analyze their reactions in response to different signals, and possibly make precise enough and experimentally verifiable predictions that can be of an extreme utility for therapeutic applications. In our studies, we focus on thermal stress and on the resulting cellular response in terms of the dynamics of the molecular species involved, but also of cell fate (death or survival) at the end of the exposure, we adress those questions by dynamic models describing the biochemical kinetics of system variables as a consequence of temperature variation. In a first step, we demonstrate through simulations, followed by experimental validation, that the temporal form of heat stress significantly impacts cell survival. This first result highlights a mechanism of saturation of the repair species as a consequence of exposure to high temperatures. In a second step, we study the potential correlation between a variability introduced on the levels of two proteins in the heat shock response network and the phenomenon of fractional killing. According to our model predictions, experimentally measured chaperone proteins (repair species) variability alone is not sufficient to explain fractional killing, which must involve other sources of variability. Finally, an analysis of the isoeffect curves generated by a generic model of the cellular response to transient stress shows the existence of four sensitivity regimes depending on the duration-intensity parameters of the stress as well as on the parameters of the response network and its time scales. Our work highlights the potential and utility of dynamic network models in the characterization of dose-response curves
Mahul, Anne-Laure. « Alix, un lien entre la voie endolysosomale et la mort cellulaire ». Grenoble 1, 2007. http://www.theses.fr/2007GRE10097.
Texte intégralAlix is an adaptor protein involved in the regulation of the endolysosomal system through binding to endophilins and CIN85, proteins involved in the receptor endocytosis and to ESCRl proteins invoJved in the endosomal function. Several observations suggest a role for Alix in controlling neuronal cell death through its interaction with ALG-2 protein. I wanted to test whether Alix may influence cell death of motoneurons (MTN) in vivo. The C-terminal part of Alix (Alix-CT) prevents carly programmed cell death (PCD) in cervical MTN at day 4,5 of chick embryo development. This effect depends 00 the Alix-Cr interaction with ALG-2 and F:SCR'r-I protein. Our resuJts suggest thar rhe interaction of the ALG-2! A!ix complex with r:SCRr proteins is necessary for the naturaIJy occurring death of M'T'N. Therefore, Alix!ALG-2 complex could make a link betwcen endosomcs and a signalling or an execution step of neuronal death. 1 have shown that the delerion of CIN85 binding site, a protein iovolved in the TNFR 1 endoeytosis, in Alix-Cr tota!!y aboJished the capacity of the latter to block rhe carly death of MTN in vivo. 1 have !iJund evidenee thar Alix funetions downstream of the dl'ath-inducing rl'cepror TNFR J, both in early MT'N dcath in (}J'O and ill vitro in cultured eells induced to die by TNFR! overcxpression, 1 have shown tha! A!ix! ALG-2 comp!ex interacts with 'rNFRJ localized on endo. ;omes. Alix, togeth. ::r with ALG-2 seems to help recruiting and activating elements of the death machinery such as caspase 8 onto "death-inducing endosomes" containing activated TNFR 1
Bouchez, Olivier. « VAD1, un régulateur putatif de la mort cellulaire hypersensible chez Arabidopsis thaliana : analyse fonctionnelle et recherche de nouvelles composantes des programmes de mort cellulaire associés à VAD1 ». Toulouse 3, 2008. http://thesesups.ups-tlse.fr/197/.
Texte intégralThe hypersensitive response (HR) is a form of programmed cell death that is commonly associated with disease resistance to pathogens, characterized by a rapid and localized cell death occurring at the inoculation site. The vad1 mutant (for Vascular Associated Death) is an Arabidopsis "Lesion Mimic" Mutant that exhibits HR-like propagative lesions along the vascular system. High expression of defense-related marker genes and increased resistance against different virulent and avirulent pathogens accompany lesion formation. Sudy of the ethylene and jasmonates-related signalling pathways using crosses between vad1 and ethylene mutants (ein2, ein3, ein4, eto2, ctr1 and 35S::ERF1) or jasmonate mutants (jar1) was performed. Results reveal that vad1-associated phenotypes were dependent on ethylene biosynthesis and signalling, while the jasmonate pathway exerts a negative regulation on vad1-associated phenotypes. In agreement with these results, an ethylene treatment of vad1 induces an acceleration of lesion formation. In addition, VAD1 expression is positively regulated by ethylene. Taken together, these results demonstrate that VAD1 acts as a negative regulator of the HR cell death. A functional study of VAD1 was then performed. VAD1 overexpression induces a delay in lesion appearance and defense transcript accumulation in Nicotiana benthamiana and in Arabidopsis plants, confirming that VAD1 acts as a negative regulator of HR and resistance. .
Babault, Nicolas. « Etude structurale du domaine PDZ de PTPN4, une cible pour le déclenchement de la mort neuronale ». Paris 6, 2011. http://www.theses.fr/2011PA066211.
Texte intégralNicolier, Magali. « Induction de l'apoptose de cellules tumorales par la staurosporine : la mitochondrie au carrefour de la mort ». Besançon, 2009. http://www.theses.fr/2009BESA0004.
Texte intégralProgrammed cell death is a group of basic physiological process, the principal one been apoptosis. A fault in this pathway is frequently complicated in both the development of tumors and their resistance to radio- and chemotherapy. However one effective therapeutic approach consists of restoring this pathway in tumors. With this context, protein tumors offer a processing target for drug development. In particular protein kinases C (PKC) are involved in several signaling pathways controlling proliferation differentiation and apoptosis. Staurosporine (STS) is a powerful inhibitor of proteins tumors capable of arresting proliferation and inducing apoptosis in numerous tumoral cell lines. Previous work in our laboratory has shown that STS induces apoptosis in cervical cancer lines (p53wt HPV+ vs p53mt HPV-) by the intrinsic apoptotic pathway. We have demonstrated that p53 plays a pivotal role in apoptose and its transcriptional activity is independent on its mitochondrial effect. In addition, we showed that cell death caused by mitochondrial effects can be achieved by molecules involved in two distinct pathways, the cytochrome c and the caspase cascade, and, AIF and a pathway independent of caspases mediated by PARP-1. The two routes are not activated at the same time according to the status of p53 (wild type vs mutant). The results presented here indicate that STS and more notably ist derivative UCN-01 may be used in future alone or in combination with other molecules to open new fields from the therapeutic intervention of cervical cancers by activating the mitochondrial apoptotic pathway
Mantini, Clea. « Identification, évolution et mort cellulaire chez un groupe de protistes, les Parabasalia ». Phd thesis, Université du Droit et de la Santé - Lille II, 2010. http://tel.archives-ouvertes.fr/tel-00578013.
Texte intégralLorrain, Séverine. « VAD1, un nouvel acteur de la mort cellulaire hypersensible chez Arabidopsis thaliana ? » Toulouse 3, 2004. http://www.theses.fr/2004TOU30060.
Texte intégralLachaud, Christophe. « Mort cellulaire induite par les sphingolipides et signalisation calcique chez les végétaux ». Toulouse 3, 2010. http://thesesups.ups-tlse.fr/1152/.
Texte intégralLCBs (Long Chain Bases) are involved in Programmed Cell Death (PCD) induced during plant-microorganism interactions. However, little is known about the mechanisms involved in LCB signaling in plants. In the present work, study of crosstalks between calcium and ROS (Reactive Oxygen Species) in tobacco BY-2 cells showed that cytosolic calcium controls both PCD and basal defence processes involving ROS, whereas nuclear calcium only controls PCD. Moreover, LCBs induce 14-3-3 phosphorylation on serine 58 and modifications of 14-3-3 targets including CPK3 in Arabidopsis thaliana cells. Interestingly, the LCB treatment leads to a calcium-dependent disruption of the CPK3/14-3-3 complex. Finally, CPK3 was identified as a kinase able to phosphorylate 14-3-3s in response to LCBs
Padrón-Barthe, Laura. « LEI/L-DNase II : mécanisme d'activation et régulation de la mort cellulaire ». Paris 5, 2006. http://www.theses.fr/2006PA05D044.
Texte intégralThe first proteases implicated in apoptosis were the caspases. But their participation in this process is no longer considered as indispensable. Other non-caspases proteases have been implicated in apoptosis, such as LEI/L-DNase II. LEI/L-DNase II belongs to the serpin superfamily. We show that LEI (antiprotease) is transformed into L-DNase II by a conformational modification. This conformational change also uncovers a nuclear translocation site, allowing this L-DNase II (endonuclease) to go to the nucleus to degrade DNA. When cells are induced with etoposide, wich does not permit the conformational change of LEI, this serpin protect cells from caspase-8 activation by indirect inhibition of cathepsin D. We have also implicated L-DNase II into two models of caspase independent cellular death : light-induced retinel degeneration and paraptosis of somato-lactotropes cells
Mehlen, Patrick. « Les petites protéines de stress : des protéines qui contrôlent la mort cellulaire ». Lyon 1, 1995. http://www.theses.fr/1995LYO10275.
Texte intégralMartel, Cecile. « Proliferation cellulaire, differenciation et mort cellulaire programmee : role des regulateurs nucleaires c-myc et rb dans les cellules epitheliales ». Paris 7, 1996. http://www.theses.fr/1996PA077342.
Texte intégralDupont, Nicolas. « Voies de signalisation cellulaire impliquées dans les étapes précoces de l'infection par Shigella flexneri dans les cellules épithéliales : rôle des débris membranaires de la vacuole de Shigella flexneri dans la signalisation de la cellule eucaryote ». Lille 2, 2009. http://www.theses.fr/2009LIL2S054.
Texte intégralLam, David. « Etude mutationnelle des morts cellulaires non-apoptotiques dans le modèle dictyostelium ». Aix-Marseille 2, 2007. http://theses.univ-amu.fr.lama.univ-amu.fr/2007AIX22104.pdf.
Texte intégralThree major types of cell death have been described in mammalian cells, apoptosis, necrosis and autophagic cell death. The protist Dictyostelium discoideum, which bears only one gene encoding for a member of the caspase family (the paracaspase gene), provides a tractable model for the study of caspase-independent non-apoptotic types of cell death. Investigations in Dictyostelium benefit from the favorable experimental and genetic properties of this model organism including a small, sequenced and haploid genome. This organism undergoes developmental cell death. In in vitro monolayer conditions mimicking this developmental death, and upon activation with the differentiation factor DIF, starved wild type Dictyostelium cells underwent autophagic vacuolar cell death (ACD). Inactivation of the autophagy gene atg1 revealed another type of death, which turned out to be necrotic cell death (NCD). In this study, we demonstrate the non-involvement of paracaspase in NCD (previously shown for ACD), and the absence of any bcl-2 family members in the Dictyostelium genome. Thus, the non-apoptotic cell death mechanisms in Dictyostelium can function in the absence of apoptosis machinery. By random insertional mutagenesis, we showed that the iplA gene, the only gene in Dictyostelium encoding the inositol 1,4,5-trisphosphate receptor (IP3R), is involved in ACD through a calcium-dependent pathway, but is only partially required for NCD. Altogether, these results contribute to define molecular mechanisms leading to non-apoptotic types of cell death in Dictyostelium
Réa-Boutrois, Angela. « Lentivirus et apoptose : rôle des protéines accessoires et régulatrices Nef, Vpr, Vpx et Tat dans la mort cellulaire ». Lyon 1, 2008. http://www.theses.fr/2008LYO10110.
Texte intégralApoptosis of uninfected CD4+ T cells is the hallmark AIDS progression during HIV and SIV infection. To study the role of Nef, Vpx and Vpr proteins in cell death of uninfected T CD4+ cells, we used recombinant of caprine arthritis encephalitis virus (CAEV) which express vpr/vpx or nef genes from SIV virus. We demonstrate that recombinant viruses can replicate in caprine cells but do not infect human or caprine T cells. In addition, we showed that the parental CAEV virus induced only apoptosis in caprine infected cells through the intrinsic pathway and that the viral Tat protein was involved in this apoptosis induction. Using chimera viruses, we demonstrated that SIV Vpr/Vpx proteins induce apoptosis of uninfected T CD4+ cells through both intrinsic and extrinsic pathways and can activate the unfolded protein response (UPR) in these cells. Moreover; SIV Nef protein expression in infected caprine cells activates the expression of soluble factor(s) that can promote apoptosis of uninfected bystander T CD4+ cells. Taken together, these results contribute to demonstrate the major role of SIV accessory proteins in the depletion of T CD4 cells
Rivière, Marie-Pierre. « Étude des fonctions intercellulaires impliquées dans la résistance liée à l'âge chez Nicotiana tabacum vis-à-vis de l'oomycète pathogène Phytophthora parasitica ». Nice, 2006. http://www.theses.fr/2006NICE4018.
Texte intégralCagnol, Sébastien. « Contrôle de la mort cellulaire par la voie des MAPK1/3 (ERK2/1) ». Phd thesis, Université de Nice Sophia-Antipolis, 2005. http://tel.archives-ouvertes.fr/tel-00104792.
Texte intégralPinan-Lucarré, Bérangère. « Autophagie dans la mort cellulaire par incompatibilité et le développement chez Podospora Anserina ». Bordeaux 2, 2005. http://www.theses.fr/2005BOR21290.
Texte intégralIn the filamentous fungus Podospora anserina, cells resulting from somatic fusions between two genetically different strains are destroyed through a cell death reaction. This cell death reaction is associated with an intense vacuolization of the cytoplasm and named death by incompatibility. High level of autophagy, an intracellular digestion process, was demonstrated during incompatibility by observing numerous and large autophagosomes. Investigating PaATG1 and PaATG8 genes, implicated in the autophagic process, revealed that autophagy is not essential to this cell death reaction. Acceleration of cell death in deltaPaATG mutant strains suggests that autophagy could be protective rather than causal during incompatibility. PaATG-independant cell death in these mutant strains is still associated with an intense vacuolization of the cytoplasm and is thus a vacuolar and non-autophagic cell death
Reix, Stéphanie. « Ré-évaluation des mécanismes de mort cellulaire programmée associée à la maladie d'Alzheimer ». Aix-Marseille 2, 2006. http://theses.univ-amu.fr.lama.univ-amu.fr/2006AIX22086.pdf.
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