Tesis sobre el tema "Division et mort cellulaire"
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Op, De Beeck Anne. "Etude du mode d'action cytotoxique de la protéine non structurale NS1 du parvovirus oncolytique MVMp: interférence avec la division cellulaire ou Chronique d'une mort annoncée". Doctoral thesis, Universite Libre de Bruxelles, 1996. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/212389.
Texto completoFarinas, Benoît. "L'algue Ostreococcus tauri, modèle émergent pour la caractérisation des principaux acteurs du cycle de division et de la mort cellulaire programmée dans la lignée verte". Perpignan, 2006. http://www.theses.fr/2006PERP0699.
Texto completoThe unicellular marine alga Ostreococcus tauri (Prasinophyceae) diverged early in evolution of green plants. O. Tauri has a very simple cellular organisation, a simple binary division and a minimal yet complete set of cell cycle control genes. Heterotrophic growth in darkness was investigated but no proliferation of O. Tauri was observed with the carbon sources tested. However, glycerol increased survival in the dark, albeit without cell division. In all conditions, cell death was observed and our results suggest occurrence of programmed cell death. Cell culture techniques were developed to optimise further work, for example for gene expression studies. Axenic cultures, with natural synchronisation by light/dark cycles was necessary for studying cell cycle regulation. O. Tauri division appeared to be fairly typical of eukaryotes. A PSTAIRE-type CDK (CDKA in plants) in the O. Tauri genome was found to be implicated in cell division. The relevant mRNA and proteins were present constitutively but with a peak of histone H1 activity early in cell cycle, suggesting a role in the G1/S transition and perhaps in the G2/M transition. As in other members of the plant kingdom, O. Tauri possesses a B-type CDK, highly regulated throughout the cell cycle, with a kinase activity occurring after OtCDKA activation, suggesting a mitotic role of OtCDKB. Although the PSTAIRE-type CDK is phosphorylated to inhibit the G2/M transition in animals, surprisingly, a tyrosine phosphorylation was detected only on OtCDKB
Chalabi, Asma. "Processus d'analyse dynamique pour l'imagerie de cellules vivantes permettant la détection des réponses cellulaires aux anticancéreux, par traitement de l'image et du signal et apprentissage automatique profond". Electronic Thesis or Diss., Université Côte d'Azur, 2024. http://www.theses.fr/2024COAZ6004.
Texto completoCell division and cell death are the main indicators to evaluate cancer drug action, and only their accurate measures can reveal the actual potency and efficacy of a compound. The detection of cell division and cell death events in live-cell assays has the potential to produce robust metrics of drug pharmacodynamics and return a more comprehensive understanding of tumor cells responses to cancer therapeutic combinations. Knowing precisely when a cell death or a cell division occurs in a live-cell experiment allows to study the relative contribution of different drug effects -such as cytotoxic or cytostatic effects, on a cell population. Yet, classical methods require dyes to measure cell viability as an end-point assay with whole population counts, where the proliferation rates can only be estimated when both viable and dead cells are labeled simultaneously.Live-cell imaging is a promising cell-based assay to determine drug efficacies, with the main limitation being the accuracy and depth of the analyses to detect and predict automatically cellular response phenotypes (cell death and division, which share some morphological features).This thesis introduces a method integrating deep learning using neural networks, and image and signal processing to perform dynamic image analyses of single-cell events in time-lapse microscopy experiments of drug pharmacological profiling. This method works by automatically tracking the cells, extracting radiometric and morphologic cell features, and analyzing the temporal evolution of these features for each cell so as to detect cellular events such as division and cell death, as well as acquiring signaling pathway dynamics.A case of study comprising the analyses of caspase-8 single-cell dynamics and other cell responses to cancer drugs is presented. The aim is to achieve automatically, at a large scale the necessary analyses to augment the phenotype prediction method available in the lab (Fateseq) and to apply it to various cancer cell lines of a human cancer cell line panel to improve our live-cell OMICS profiling approaches, and, in a longer term, to scale up pharmacological screening of new cancer drugs
FERNANDEZ, PIERRE-ALAIN. "Analyse cellulaire et moleculaire de la mort cellulaire programmee des vertebres". Paris 6, 1995. http://www.theses.fr/1995PA066321.
Texto completoDEPRAETERE, 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.
Texto completoRaoul, Cédric. "Mort développementale et pathologique du motoneurone spinal : Implication du récepteur de mort Fas (CD95)". Aix-Marseille 2, 2002. http://www.theses.fr/2002AIX22018.
Texto completoMorel, 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.
Texto completoMoreira, Wilfried. "Stress oxydatif, différentiation et mort cellulaire chez le parasite Leishmania". Thesis, Université Laval, 2011. http://www.theses.ulaval.ca/2011/28186/28186.pdf.
Texto completoOizel, 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.
Texto completoTumor 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
Larmonier, Nicolas. "Mort des cellules cancereuses et réponse immunitaire antitumorale". Dijon, 2004. http://www.theses.fr/2004DIJOMU01.
Texto completoDrian, 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.
Texto completoRéa-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.
Texto completoApoptosis 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
Mahul, Anne-Laure. "Alix, un lien entre la voie endolysosomale et la mort cellulaire". Grenoble 1, 2007. http://www.theses.fr/2007GRE10097.
Texto completoAlix 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
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.
Texto completoOne 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.
Texto completoOne 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
Martel, 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.
Texto completoSouissi, 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.
Texto completoSTAT3 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
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.
Texto completoLachaud, Christophe. "Mort cellulaire induite par les sphingolipides et signalisation calcique chez les végétaux". Toulouse 3, 2010. http://thesesups.ups-tlse.fr/1152/.
Texto completoLCBs (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.
Texto completoThe 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
Anne, Sandrine. "Mort neuronale et cycle cellulaire : Rôle de la huntingtine et de ses modifications post-traductionnelles". Paris 11, 2007. http://www.theses.fr/2007PA11T083.
Texto completoPinan-Lucarré, Bérangère. "Autophagie dans la mort cellulaire par incompatibilité et le développement chez Podospora Anserina". Bordeaux 2, 2005. http://www.theses.fr/2005BOR21290.
Texto completoIn 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
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/.
Texto completoThe 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. .
Imbeault, Emilie. "Le rôle du récepteur NOD-like, Nlrx1 dans la neuroprotection et la mort cellulaire". Mémoire, Université de Sherbrooke, 2015. http://hdl.handle.net/11143/6937.
Texto completoAbstract : Neuronal cell death is a phenomenon that occurs during brain development as well as in pathological diseases. Depending on the environment in which the cells are; a poptosis or necrosis can contribute to neuronal cell death. Necrosis produces an environment that promotes inflammation and cytotoxicity and apoptosis is a highly organized process that maintains tissue homeostasis. A recently discovered NOD receptor, Nlrx1, is thought to play a role in regulation of inflammation and cell death during infection. Therefore, we hypothesize that Nlrx1 plays a neuroprotective role by controlling cell death in neurons. To determine the protective mechanism of Nlrx1 in vitro, a Knock-Down, a Knock-In and a Scrambled control of Nlrx1 in N2a cells was generated. LDH assays for cell death detection with staurosporine or oxidative stress, such as rotenone, MPP+ or H[subscript 2]O[subscript 2], have been done. After 24h treatment of staurosporine, N2a Knock-In cells showed higher cell death than N2a Knock-Down and Scrambled. When cells were treated with rotenone or H[subscript 2]O[subscript 2], N2a Knock-In cells had less cell death than Scrambled cells. N2a Knock-Down cells resulted in more cell death than Scrambled cells when treated with rotenone or MPP+.Western Blotting of HSP90 and HMGB1 as well as flow cytometry of cell death demonstrated N2a Knock-In cells to have less necrotic cells when treated with rotenone compared to Scrambled. The ratio of necrotic cells on apoptotic cells was also higher in N2a Knock-Down cells compared to Scrambled cells. Electron microscopy of control cells showed that Knock-In cells contains more mitochondria than Knock-Down and Scrambled cells. These results were confirmed by mitotracker staining by flow cytometry. Western blotting showed that there was an increased in Knock-In cells of active phosphorylated-DRP1 protein, a protein implicated in mitochondrial fission. Thus, it could explain the increased number of mitochondria seen in Knock-In cells. Immunoprecipitation showed that Nlrx1 protein interacts with DRP1 as well as active phosphorylated-DRP1. Adding Mdivi, a mitochondrial fission inhibitor, to rotenone or H[subscript 2]O[subscript 2] treatments, cell death was increased in Knock-In cells compared to Scrambled. Also, necrosis was also augmented in Knock-In cells to levels comparable to Scramble and Knoc k-Down cells. These results suggest an implication for Nlrx1 in regulating the balance of necrosis to apoptosis, permitting cells to survive. Nlrx1 could serve as a neuroprotective molecule in diseases mediated by oxidative stress.
Pajaud, Julie. "Rôle modulateur de la glutathion transférase Pi dans la prolifération et la mort des cellules normales et transformées". Thesis, Rennes 1, 2013. http://www.theses.fr/2013REN1S175/document.
Texto completoIncreased GSTP1 expression is frequently observed in cancers and is positively correlated with chemotherapy resistance. This phase II detoxifying enzyme can also regulate JNK and TRAF2 activities and, consequently, can modulate proliferation and cell death pathways. This project aimed at studying the role of GSTP1 during proliferation in normal and transformed hepatocytes. Liver regeneration study in Gstp1/2‐/‐ mice showed the involvement of GSTP1 and GSTP2 proteins in the cell cycle progression control of normal hepatocytes. After partial hepatectomy in Gstp1/2‐/‐ mice, the number of cells in S, G2 and M phases was decreased compared to livers of wildtype mice. This reduction is associated with the delay in the expression of proteins involved in proliferation initiation, mitogen restriction point control and G1/S transition. These modifications are associated with the decrease in TRAF2 expression and the activation of JNK and ERK, whereas p21 and p53 levels are high. Furthermore, expression of enzymes involved in redox homeostasis and MAPK activation is delayed. Study of cells derived from various cancers, including HCC, highlighted a correlation between low expression of GSTP1 and decrease in cell proliferation without cell survival alteration. However in these conditions, we observed the increase in TRAF2, pJNK, pATF2 and ATF3 expression together with the induction of p21. We also showed that GSTP1 effects are regulated by JNK activation. These results showed a link between GSTP1 expression and hepatocyte proliferation and led us to investigate the GSTP1 expression in HCC. We noticed an induction of GSTP1 expression in peritumoral tissue compared to normal liver
Hérincs, Zoltán. "Dissection des événements proximaux dans les signaux de mort cellulaire engendrés par les récepteurs Fas et DCC : rôles des microdomaines membranaires et de la palmytoylation". Nice, 2005. http://www.theses.fr/2005NICE4067.
Texto completoFas (CD95), a prototype of the superfamily of TNFRs (tumor necrosis factor receptor), is a key receptor inducing cell death. Most of human tumor cells present modifications in Fas and/or FasL expression, and the activity of this receptor was shown to be involved in treatments used in cancer therapy. Recently, Fas-triggered non-apoptotic signals (i. E. NF-κB) have been shown, in contrast to cell death signals, functional in tumor cells. Our team's main objective is to dissect proximal membrane mechanisms that control the balance between apoptotic and non-apoptotic Fas-mediated pathways in order to restore cell death in tumor cells. This PhD thesis provides evidence for the pivotal role of specialized regions of the plasma membrane, i. E. , "rafts", in Fas-based signalisation. We also show that (i) the association between Fas and the ezrin protein is a crucial initiating step of receptor internalization following ligand binding, and that this event is not only necessary to the death signal but is required to the "death-inducing signaling complex" formation; (ii) Fas/ezrin association depends on Fas palmitoylation; (iii) Fas-induced non-apoptotic pathways, in contrast to death pathways seem to be independent of receptor internalization : the molecular dissection of the factors controlling this step (and associated drugs) could be used as new tools in cancer therapy
Strappazzon, Flavie. "Mécanismes d'action d'Alix et de ses partenaires ALG-2 et PYK2 dans la survie et la mort neuronale". Grenoble 1, 2007. http://www.theses.fr/2007GRE10250.
Texto completoLn an effort to uncover the molecular mechanisms underlying the function of Alix and AIg-2 in cell death, we have found that Alix and AIg-2 can Ca2+-dependently associate with caspase-8 in BHK-21 cells. We investigated the possible existence of an Alix! AIg-2-caspase-8 relationship during cerebellar granule neuron death induced in vitro byeither potassium depletion or Alix overexpression. We showed that Alix is found in a caspase-8-containing complex following K+ depletion-induced CGN apoptosis. Moreover, we demonstrated that caspase-8 functions as initiator caspase in the apoptotic pathway induced by Alix overexpression. Ln a recent work, we gained evidence that the dosure of these Ca2+ channels, which follows the shift to K5 medium,could trigger compensatory Ca2+ mobilization from intracellular stores (Strappazzon, 2007). This prompted us to tum our attention to the putative functional relevance of Alix!Alg-2-caspase-8 interaction to ER stress-induced death. Using both dividing BHK-21 cells and post-mitotic CGN exposed to the ER stressor thapsigargin, we gathered several evidence supporting the idea that Alix, like its binding partner AIg-2, is involved in ER stress-induced death, linking specifficaly two initiator caspases: caspase-8 and -9. Overall our findings suggest that Alix, through its association with AIg-2, is a key mediator of the apoptotic Ca2+ signaling machinery. We also demonstrates the role of Pyk2 in mediating the trophic effect of membrane depolarization in CGN and its possible involvement in survival via the regulation of the binding between Alix and AIg-2 through phosphorylation of Alix
Deluche, Cynthia. "Endoréduplication, division et expansion cellulaire : mécanismes acteurs de la croissance du fruit". Thesis, Bordeaux, 2015. http://www.theses.fr/2015BORD0199/document.
Texto completoThe transformation of the ovary wall into a fleshy pericarp involves a coordinated pattern of cell division and cell expansion. Considerable data have been reported on tomato fruit development and ripening, but the pattern of cell division, cell expansion and endoreduplication at the tomato fruit set and during fruit growth remains grossly appreciated at the whole pericarp level and many questions are not yet resolved: How are cell division and cell expansion coordinated in tomato fruit a cellular level and according to developmental time? When does endoreduplication begin in fruit tissues and what is its function? The first part of this deals with the coordination of cell division and cell expansion during the end of tomato ovary development and the beginning of fruit growth. Evidence for early differentiation of cell layers in the ovary wall and then in fruit pericarp are presented. Cell division happens mainly in the external epidermis and shows partial synchronization, whereas cell expansion happens mostly in mesocarp cell layers. Endoreduplication is initiated as soon as before anthesis. The second part of this work is devoted to RNA-seq based transcriptome profiling of pericarp nuclei which have been sorted according to four ploidy levels (4, 8, 16 and 32C). We demonstrate that the expression of most of the pericarp-expressed genes shows a proportional increase according to ploidy level, on a nuclear basis. However, a significant amount of genes has been identified as over-expressed or under-expressed according to ploidy level
Rannou, Yoann. "Contrôle de la division cellulaire par les protéines kinases Mnk1 et Aurora". Rennes 1, 2008. http://www.theses.fr/2008REN1S123.
Texto completoDuring mitosis two genetically identical daughter cells are generating. Mitosis is tightly controlled by various proteins like kinases in order to avoid errors which can lead to chromosomal instability. The aim of my PhD was to identify new kinases involved in mitosis control. I have identified the Mnk1 kinase which allows cell abscission by recruiting the centriolin at the midbody. I have also showed that the N-terminal domain of Aurora-A kinase regulates its localization at centrosomes, whereas Aurora-B N-terminal domain facilitates its nuclear localization. Finally I have described a new Aurora-A function. This kinase phosphorylates the Numb protein, a cell fate determinant involved asymmetric division. Numb phosphorylation by Aurora-A could control its localization and/or its endocytic activity
Meï, Coline. "Etude des relations entre division cellulaire et métabolisme des triglycérides chez les plantes et les microalgues". Thesis, Université Grenoble Alpes (ComUE), 2016. http://www.theses.fr/2016GREAV043/document.
Texto completoAlternatives to fossil fuel are one of the biggest challenges of the 21st century. Plants and microalgae are able to produce oil which is easily convertible in biodiesel. In order to optimise the biofuel production it is necessary to know the cellular mechanisms leading to the setting up of these storage lipids or TAG (Triacylglycerides). In its physiological condition, the lipid flux is naturally orientated towards the membrane lipid synthesis, which allows the creation of new membranes which occurs during the cell division. Nitrogen deficiency, a condition often encountered by plants and algae, is known to induce cell growth to slow down and an accumulation of TAG in microalgae models. Is the lipid flux, which is conventionally orientated towards new membrane synthesis, tipped over the storage lipid synthesis? To check this hypothesis, a range of compounds known to stop the cell growth was tested on the higher plant model Arabidopsis thaliana, according to a chemical genetic strategy. All treatments showed a rise of the TAG content associated to a cell growth inhibition. Among them, the methotrexate inhibit the dihydrofolate reductase enzyme involved in the C1 metabolism and induced a TAG accumulation up to 15 times the control. This treatment was compared to a nitrogen starvation condition, which in our experiments slowed down the cell growth and induced an increase of 60 times to the TAG content. The lipid profile analysis revealed that the nitrogen deficiency led to a decrease of membrane lipids -phospholipids and galactolipids, in favour to TAG, whereas the methotrexate treatment was not associated to any membrane remodelling. Nevertheless, both conditions shared similarities, as the modifications of the fatty acid insaturation profile and the expression of desaturase genes. The strong gene expression of Non Specific phospholipases C (NPC4/5) and pulse-chase experiments performed with a labelled phosphatidylcholine (PC), highlighted the predominant involvement of this phospholipid in the TAG production which occurs during the two treatments. In order to evaluate the NPC role in the storage lipid metabolism more closely, A. thaliana mutant lines for NPC4 and NPC5 (over-expressers and knock-out) were initiated. Microalgae are powerful models for the third generation of biofuels. For this reason we tested the impact of a nutrient deficiency as well as the effect of different growth inhibitors on the TAG accumulation in the marine microalgae Phaeodactylum tricornutum. Preliminary results suggested that the inhibitor sensibility can be different between diatoms and higher plants
Chancharme, Laurent. "Hétérogénéité des LDL et stress oxydant : stabilité des hydroperoxydes lipidiques et induction de la mort cellulaire". Paris 5, 2001. http://www.theses.fr/2001PA05P604.
Texto completoLDL play a key role during the formation and the progression of atherosclerotic lesions, more parti ularly after they undergo oxidative modifications. Moreover, LDL are present in a continuum spectrum of paricles which display differences in their physico-chemical properties and their atherogenicity, as demonstrated by the correlation between a high level of small dense LDL and an increased cardiovascular risk. In our studies, we noticed that, during oxidative modifications of LDL subfractions from normolipidemic subjects (NL), lipid hydroperoxides formed in dense LDL have a lower stability as compared to those formed in intermediate LDL. .
Villalpando-Rodriguez, Gloria-Elisa. "Le rôle des calpaïnes et des lysosomes dans la mort cellulaire indépendante des caspases". Paris 6, 2012. http://www.theses.fr/2012PA066339.
Texto completoIn a light induced retinal degeneration model (lird), studied in our laboratory the activation of autophagy and calpaîns have been shown : The aim of my work was to study the response of rpe during stress and to explain the role of calpains in photorecptors death. We have shown that metabolic sterss of rpe cells, in culture, induce autophagy activation. During the first 2 hours; this autophagy protects cells, but, afertwards the same mechanism triggers cell death. We have also shown that calpain 1 permeabilises lysosomes by degradation of the lysosomal associated protein 2. The same protein cleavage has been observed in lird. Moreover, calpain 2 can activate an acidic calpain dependent endonuclease that could be implicated in dna degradation of dying cells. It would be interesting to study the effects of calpain 1 inhibition during lird, as well as in other neural cell death models. The complete caracterisation of the calpain dependent endonuclease could provide more information on caspase-independent cell death mechanisms, highly involved in retinal degeneration
Forcet, Christelle. "Le récepteur à dépendance DCC : carrefour entre le guidage axonal et la mort cellulaire". Lyon 1, 2002. http://www.theses.fr/2002LYO10069.
Texto completoHadife, Nader. "Interleukine-24 : rôle immunologique et mécanismes d'induction de mort cellulaire dans les lymphocytes B". Thesis, Université de Lorraine, 2013. http://www.theses.fr/2013LORR0018/document.
Texto completoWe have previously shown that Interleukin(IL)-24 a class-II cytokine of the IL-10 family has cytostatic and cytotoxic properties on normal and malignant human B-cells previously engaged into the cell cycle, but not on quiescent B-cells. IL-24 also inhibits the differentiation of germinal center B-cells in plasma cells in an in vitro model; the later was used to compare for the first time the transcriptome of B-cells cultured or not with IL-24 for 6 and 36h. Several "early" transcripts involved in DNA metabolism and replication were inhibited whereas that of Igf1 a molecule described as a B-cell growth factor was induced. We show herein that IgF1 has instead a proapoptotic role on B-cells at physiological concentrations. In contrast, several genes of the intrinsic apoptotic pathway were stimulated after 36h. This expression pattern was also found in CLL cells whether they were "IgVH mutated" or "unmutated", albeit with distinct kinetics from normal B-cells. In addition several genes belonging to the immune synapse and innate immunity were regulated by IL-24. These results disclose additional, possibly immunoregulatory properties, for IL-24 than its already described cytostatic and potentially anti-tumoral effects
Pradelli, Ludivine. "Rôle du métabolisme glycolytique dans la régulation de la mort cellulaire dépendante et indépendante des caspases". Nice, 2010. http://www.theses.fr/2010NICE4039.
Texto completoEfthimiadi, Laurie. "Mort programmée induite par le NMDA dans l'hippocampe et lien avec la reprise du cycle cellulaire". Aix-Marseille 2, 2008. http://theses.univ-amu.fr.lama.univ-amu.fr/2008AIX22023.pdf.
Texto completoBordeaux, Marie-Claire. "Caractérisation de deux nouveaux récepteurs à dépendance, RET et TrkC". Lyon 1, 2003. http://www.theses.fr/2003LYO10093.
Texto completoVoisin, Laurent. "Caractérisation des bases moléculaires et cellulaires de l'Entose". Thesis, Université Paris-Saclay (ComUE), 2016. http://www.theses.fr/2016SACLS439.
Texto completoMy research reveals a new signaling pathway which is involved in the cellular internalization. This signaling pathway requires ATP release and purinergic receptor activation at the level of cannibal cells and will lead to the elimination of internalized cell. We also defined during this work the future of the cannibal cell and specify during experiments in vivo the tumor suppressor activity of cellular cannibalism. We also observed this process in tumor biopsies obtained from patients with breast cancer who received neoadjuvant treatment and have revealed that its detection could predict the efficacy of neoadjuvant treatment. Theses results reveal molecular bases of cellular cannibalism and indicate the role of cellular cannibalism during tumor development
Cabon, Lauriane. "Implication d'AIF dans la mort cellulaire et la physiologie mitochondriale : exemples dans la nécroptose intrinsèque et l'hématopoïèse". Thesis, Paris 6, 2014. http://www.theses.fr/2014PA066314/document.
Texto completoAIF is one of the cell death effectors released from mitochondria but it also possess a vital role by regulating the cellular respiration. Throughout this thesis work, I have focused my studies on these two functions. On one hand, I have performed a deeper characterization of the DNA alkylating agent induced regulated necrosis. I have identified RIP1 as a crucial determinant of this cell death pathway, hence linking it to necroptosis. I have also highlighted the role of BID, a BH3-only member of the BCL-2 family, in the mitochondrial release of AIF. I have shown that calpains proteases cleave BID into tBID which relocalize to mitochondria where it helps activating the pro-apoptotic factor BAX. This study contributes to reconsider the role of BH3-only proteins in cell death pathways beyond apoptosis. On the other hand, I have studied AIF role in hematopoiesis thanks to a mouse model with hematopoietic lineage-specific deletion of AIF. I have observed a block in T-cell development and the rapid development of severe pancytopenia. I have demonstrated that this pancytopenia is associated with the loss of hematopoietic stem cells whom capacities were tested both ex vivo and in vivo. In order to understand the underlying determinants of these defects, I have characterized the cellular consequences related to AIF deletion : loss of the respiratory chain complex I, decrease of the oxidative phosphorylation capacity, decreased levels of ATP, increased levels of reactive oxygen species. This second study reveals the importance of a proper oxidative phosphorylation system combined with healthy mitochondria for a normal hematopoiesis and hematopoietic stem cells maintenance
Geffroy, Alexandrine. "Régulation de la mort et survie des plasmocytes humains normaux et de leurs équivalents tumoraux, les cellules du myélome multiple". Nantes, 2007. https://archive.bu.univ-nantes.fr/pollux/show/show?id=08d09692-c5dc-4de8-ae3b-1188e081bc4a.
Texto completoPlasma cells are terminally differentiated final effectors of the humoral response. Plasma cell differentiation is characterized by extensive apoptosis. By this way, plasma cell homeostasis is maintained in vivo. The aim of this study was to improve our knowledge about mechanisms underlying cell survival and apoptosis during plasma cell differentiation. We show that as early as proplasmablast stage in the time course of plasma cell differentiation, cells have entered in apoptotic process characterized by effector caspase activation (caspase-3 and -6), Mcl-1 cleavage, a marked decrease of Bcl-2 and increase of Bim EL isoform. Moreover, these cells are susceptible to Fas-mediated apoptosis but resistant to TRAIL-receptor-mediated apoptosis. We demonstrated that osteoclasts, macrophages and dendritic cells, all of monocyte origin, are able to support cell survival during plasma cell differentiation. However, osteoclasts were more potent than macrophages to support the survival of plasma cells whereas dendritic cells mediated survival of plasmablasts only. Surviving plasma cells on osteoclasts displayed phenotypic features of fully differentiated plasma cells suggesting that osteoclasts could take part to the putative bone marrow niche of plasma cells
Maisonneuve, Pierre. "Etude structurale et fonctionnelle de la phosphatase humaine PTPN4". Thesis, Paris 6, 2014. http://www.theses.fr/2014PA066673/document.
Texto completoThe function of signaling proteins is determined by the nature of the domains from which they are made up. A better understanding of cell signaling pathways will result from the study of these domains and their regulation. PTPN4 is a non-receptor tyrosine phosphatase with an anti-apoptotic function. Upon infection with an attenuated rabies virus, its function is hijacked, which subsequently leads to cell death. This phenotype is arises from the interaction of the PDZ binding motif (PBM) of the viral glycoprotein with the PDZ domain of PTPN4. In this study, we show that this PDZ domain is an allosteric inhibitor of the catalytic activity of the PTPN4 phosphatase domain. This is the first description of the regulation of a phosphatase by a PDZ domain. This inhibition is released by the interaction of a ligand to the PDZ domain, such as the viral glycoprotein PBM. Our structural study revealed that the PBM recognition disrupts the transient inter-domain interactions and restores the complete phosphatase catalytic properties. As well, we identified a PTPN4 endogenous ligand, the MAP Kinase p38, which may participate in the regulation of the cellular homeostatic through its interaction with PTPN4. Thus, in addition to its phosphatase regulatory role, the PDZ domain also allows the recruitment of partners and the introduction of substrates to the PTPN4 phosphatase active site. This study contributes to our understanding of the role played by PDZ domains in cell signaling pathways
Rousselle, Tristan. "Etude fonctionnelle de la protéine p21(waf1/cip1) : rôles joués au cours du cycle cellulaire et de la mort cellulaire programmée". Université Joseph Fourier (Grenoble), 1999. http://www.theses.fr/1999GRE10210.
Texto completoSerrano, Amandine. "Expression de GALIG, gène inducteur de la mort cellulaire, dans des cellules normales et pathologiques". Thesis, Orléans, 2017. http://www.theses.fr/2017ORLE2019/document.
Texto completoEmbedded within the GALECTIN-3 gene, GALIG gene allows the production of 2 proteins, Galigins, which interact with autophagy proteins. Described as a pro-apoptotic gene, it is inhibited by Mcl-1, an anti-apoptotic protein. It is under-expressed in the bone marrow (BM) of patients with Acute Myeloid Leukemia (AML) M2, a pathology characterized by a differentiation blocking. During my thesis, I showed that the GALIG gene could be involved in myeloid differentiation. The expression of GALIG gene gradually increases in AML with the differentiation stage of the leukemic cell. In addition, although weak at diagnosis, GALIG gene expression also increases in BM and blood after chemotherapy treatment. These observations are reinforced by in vitro studies which indicate that GALIG expression increases early during polymorphonuclear and macrophages differentiations, before the onset of terminal maturation features. Cell survival during differentiation could be ensured by the increasing expression of the MCL1 which could counteract the apoptotic function of GALIG. In the blood of treated HIV-infected patients, without viral load, the transcription rate of GALIG is higher when compared to uninfected donors. This suggests a possible dysfunction of the immune system. In addition, several autophagy genes are dysregulated which could lead to the inhibition of the basal level of autophagy in these patients, which in turn could be a cause of the premature aging of blood cells and linked to the chronic inflammation reported for efficient treated HIV patients. In conclusion, these results encourage us to pursue studies deciphering the mechanisms of regulation of the GALIG gene expression and the mechanisms of action of the Galigins
Essabbani, Abdellatif. "La clusterine : un nouveau régulateur de la voie NF-қB et de la mort cellulaire". Paris 5, 2009. http://www.theses.fr/2009PA05T025.
Texto completoClusterin: a new regulator of NF-kappaB pathway and cell death Clusterin is a multifunctional protein that plays numerous roles in mammalian cells. By mean of transcriptomic analysis, we previously demonstrated that lower expression of clu both in tissues and cultured fibroblast-like synoviocytes of rheumatoid arthritis patients compared to osteoarthritic patients. We showed that CLU interacts with phospho-IkB-a and decreases the translocation of p50/p65 to the nucleus. To specify the interaction sites of CLU with its partners and to study the CLU isoforms roles, we generated several molecular constructs coding for various CLU regions of interest and test their role on NF-қB pathway and CLU subcellular localization. We have also developed a new approach of "exon skipping" in order to induce preferential expression of the nuclear spliced form of the gene. This strategy will allow a good understanding of nuclear forme poorly characterized
Dunys, Julie. "Le complexe gamma-secrétase et la mort cellulaire par apoptose : implication dans la maladie d'Alzheimer". Phd thesis, Nice, 2007. https://theses.hal.science/tel-00316788.
Texto completoAlzheimer's disease is characterized at the histopathological level by neurofibrillary tangles, senile plaques and massive neuronal loss. Senile plaques are composed by the aggregation of amyloid-b peptide, which is produced after cleavage of a transmembrane protein, bAPP, by two enzymatic activities, named b- and g-secretases. The g-secretase activity is borne by a high molecular weight complex composed of at least four proteins, a Presenilin, Nicastrin (NCT), Pen-2 and Aph-1. The lack of one of the four members induces an inhibition of the g-secretase activity. This PhD focused on degradation processes involved in Aph-1 and Pen-2 catabolism and on the role that could play these proteins, as NCT on regulation of neuronal apoptosis. We have shown that Aph-1, Pen-2 and NCT decrease neuronal sensitivity to apoptosis by lowering caspase-3 activity. These processes are under control of p53 that expression is regulated by Aph-1, Pen-2 and NCT. Cell signalling induced by the three proteins are although different. Aph-1 and Pen-2 antiapoptotic function require integrity of the g-secretase complex, but not its activity, while NCT antiapoptotic function is independent of the complex. We examine also Pen-2 and presenilins transcription. We show here that the link between p53 and Pen-2 is not unidirectional. P53 transcription is regulated by an intracellular fragment, AICD, produced after g-secretase cleavage of bAPP. We demonstrate that AICD and p53 increase Pen-2 transcription. Otherwise, we show that Pen-2 is involved in transcriptional control of presenilins, demonstrating that members of the g-secretase complex could regulate each other's
Dunys, Julie. "Le Complexe Gamma-secrétase et la Mort Cellulaire par Apoptose : Implication dans la Maladie d'Alzheimer". Phd thesis, Université de Nice Sophia-Antipolis, 2007. http://tel.archives-ouvertes.fr/tel-00316788.
Texto completoPetitot, Anne-Sophie. "Isolement, caractérisation et étude de gènes impliqués dans les phases précoces du traitement de cellules et de plants de tabac par la cryptogéine, un éliciteur de réactions de défense". Dijon, 1997. http://www.theses.fr/1997DIJOS053.
Texto completoTOUNEKTI, OMAR. "Fragmentation de l'adn et mort cellulaire : mort mitotique, pseudo-apoptose ou apoptose suivant le nombre et le type des coupures simple ou double brin de l'adn". Paris 6, 1996. http://www.theses.fr/1996PA066416.
Texto completoMoulet, Hélène. "Mort cellulaire initiée par l'oxygène singulet : mise en évidence d'effets à longue portée". Thesis, Lille 1, 2019. http://www.theses.fr/2019LIL1R004/document.
Texto completoSinglet oxygen (1O2) is the first excited state of molecular oxygen. It is the major cytotoxic agent in photo-dynamic therapy. We use direct optical excitation of oxygen to quantitatively estimate 1O2 production rate in cells and to study its cytotoxic effects.In multicellular tumor spheroids, which mimic tumor geometry in vitro, we highlight long-range cell death that cannot be explained by singlet oxygen alone. This death is caused by 1O2 generated within spheroids but outside of the cells. We set up an experiment enabling spatial control of extra-cellular 1O2 production. The measured long-range cell death in these experiments implies the presence of secondary reactive oxygen species. Lastly, some cell death modalities are preferred from a treatment perspective, in order, for example, to limit inflammatory response. We set up an in vitro experiment that enabled us to observe different cell death modalities according to 1O2 production rates and exposure times
Giaime, Emilie. "Mort cellulaire et Maladie de Parkinson : Rôle de la synphiline-1, de la Parkine et de DJ-1". Phd thesis, Université de Nice Sophia-Antipolis, 2008. http://tel.archives-ouvertes.fr/tel-00421102.
Texto completoJe me suis consacrée à l'étude de leurs fonctions physiologiques, ainsi qu'à leurs implications dans les processus apoptotiques. Ainsi, j'ai déterminé que ces protéines réduisent l'activité de la caspase-3 induite par différents stimuli. Ce rôle protecteur passe par la régulation de la voie dépendante de p53. De plus, j'ai identifié DJ-1 et la synphiline-1 comme étant substrats des caspases, mais aussi que les fragments C-terminaux issus de ce clivage portent leurs activités biologiques.
Parallèlement, j'ai étudié des aspects de la régulation transcriptionnelle de DJ 1 et de la PK par le facteur de transcription p53. J'ai mis en évidence une boucle de régulation entre p53, DJ-1 et la PK. J'ai montré que ces deux protéines sont capables de réguler l'expression de p53. De plus, j'ai déterminé que la PK régule positivement DJ-1, et que ce contrôle s'effectue via la régulation transcriptionnelle de DJ-1 par p53.