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Дисертації з теми "Cycle cellulaire – Dissertations universitaires":
Cariou, Sandrine. "Mecanismes controlant la progression en g1 et la transition g1/s du cycle cellulaire des hepatocytes normaux et transformes." Paris 5, 1996. http://www.theses.fr/1996PA05S010.
Gautier, Thierry. "Analyses biochimique et moleculaire de la peripherie des chromosomes dans les cellules de mammiferes : une etude au moyen d'autoanticorps humains pendant le cycle cellulaire." Paris 5, 1993. http://www.theses.fr/1993PA05S009.
Obiang, Linda. "Rôles des partenaires cellulaires de la protéine de matrice du virus de la stomatite vésiculaire dans le cycle viral." Paris 7, 2011. http://www.theses.fr/2011PA077044.
The matrix protein (M) of vesicular stomatitis virus (VSV) is a multifunctional 26,6 kDa small protein. M protein plays a key role in assembly and budding processes and is responsible for cellular synthesis shut down, microtubules destabilization and apoptosis. For these reasons, M protein recruits several cellular partners. Among cellular proteins identified so far, we are interested in Nedd4, E3 unbiquitin ligase and TSG101, a component of ESCRT I complex. 2-Yeast Hybrid technique allowed us to identify three news partners for M protein: Dynamin, protein involved in endocytic pathway, LMP2, catalytic subunit of immunoproteasome and Catenin a, that belongs to intercellular junctions. First, we studied the implication of Nedd4, TSG101 and dynamin during late stages of the viral cycle: assembly and budding. We characterized recombinants mutant virus containing matrix protein that does not interact anymore with one or two partners. For that, we developed a new technique to titrate with higher accuracy viral supernatants. We applied this technique for growth curves in different cell type. Our results" suggest that TSG101 plays a role during budding that highlighted with double mutant virus. EM observations indicate that dynamin acts upstream Nedd4. We also showed that some viral particles produced from an infection using virus containing M protein that does not interact with Nedd4 display an aberrant morphology and their M protein is no longer ubiquitinated. After, we started the study of new partners of M protein: LMP2 and Catenin a, previously identified. We expressed these proteins in fusion with GST and we have shown that these buildings were well able to interact with the M, confirming both interactions. Finally we could define residues and domains involved in M-LMP2 and M-Catenin a interactions. Preliminary experiments show that M protein and Catenin a colocalize at level of epithelial cells membrane. An results contribute to a better understanding of the interactome complex matrix protein
Labit, Hélène. "Régulation de l'initiation de la réplication chez les vertèbrés : analyse du programme temporel d'activation des origines de réplication dans les extraits d'oeufs de xénope." Paris 7, 2007. http://www.theses.fr/2007PA077176.
In Vertebrates, replication origins are activated according to a spatial and temporal program. In early Xenopus embryos, origins are located at apparently random sequences and are activated in clusters that fire at different times throughout S phase. The main object of the present work is to characterize the temporal regulation of replication in Xenopus egg extracts through analysis of origin activation on single DNA fibers and replication foci distribution in sperm nuclei. Using molecular combing of DNA, we compared the distributions of replication origins fired at the beginning of two following S phases. Absence of significative coincidence between origins shows that the temporal order of replication does not depend on genomic position. Furthermore, no epigenetic central regulates the moment of origin firing. However the detection of coincidence between replication foci labeled at the beginning of two following S phases suggests that the chromosomal organization may influence the replication timing. Using FISH, we showed that the replication of the ribosomic DNA is delayed compared to the replication of whole genomic DNA. An altered chromatin structure may be responsible for this delay. Mapping of origins revealed that initiation frequency is two fold lower in the G+C rich intergenic spacer than in the coding rDNA sequence. At the rDNA, local parameters such as nucleotide composition may influence the localization of replication origins
Deleye, Yann. "Rôle du gène suppresseur de tumeur p16INK4a dans le métabolisme hépatique des lipides au cours du jeûne." Thesis, Lille 2, 2018. http://www.theses.fr/2018LIL2S002.
P16INK4a is a tumor suppressor protein that is a well described cell cycle regulator. Recently, genome-wide association studies (GWAS) associated the CDKN2A locus, from which p16INK4A is encoded, with increased risk for development of type 2 diabetes. A pathophysiological link between p16INK4a and hepatic glucose homeostasis has been unraveled recently, through the control of gluconeogenesis. Patients with T2D also present with disturbances in fat metabolism, associated with an increased prevalence to Non Alcoholic Fatty liver diseases (NAFLD). In this context, we investigated the role of p16INK4a in hepatic lipid metabolism in vitro using primary hepatocytes, the murin AML12 and human IHH hepatocyte cell line transfected respectively with siRNA-CDKN2A and siRNA-p16 and in vivo using p16+/+ and p16-/- mice.Transcriptomic analyses of p16+/+ and p16-/- primary hepatocytes using microarrays revealed that metabolic and PPARα signaling pathways were among the most modulated in p16 absence. Moreover, in primary hepatocytes and in hepatocyte cell lines, p16 deficiency modulates a subset of PPARα target genes associated to fatty acids oxidation (FAO). These effects were associated with an increased response to GW647, a PPAR945; agonist, and reversed by siRNA targeting PPAR45;. Investigating known PPAR945; activators and transcriptional co-activators in vitro, we found that upregulation of FAO genes expression was linked to SIRT1. AMPK is a known activator of FAO and has been shown to induce SIRT1 activation through increase of NAD/NADH ratio. Interestingly, downregulation of p16 expression in vitro led to increased AMPK phosphorylation and activation.In vitro, p16-/- primary hepatocytes demonstrated enhanced fatty acid oxidation of oleate compared to p16+/+. During fasting, enhanced FAO leads to a shift of acetyl-coA utilization from the TCA cycle to ketogenesis. Interestingly, p16-/- mice showed a tendency to produce more ketone bodies than their control littermate after sodium octanoate injection. These findings describe a new function for p16INK4a in hepatic lipid metabolism through activation of AMPK-SIRT1-PPARα pathway
Baccini, Véronique. "Polyploïdisation des mégacaryocytes : Rôle de P21cip1 et P27kip1 et de la voie de signalisation mammalian Target of Rapamycin (mTOR)." Paris 7, 2007. http://www.theses.fr/2007PA077180.
Megakaryocyte differentiation is characterized by polyploidization of progenitors and cell size increasing. The term of differentiation is controlled by thrombopoietin (TPO) which stimulates various types of intracellular signaling pathways. The aim of my thesis was to understand mechanisms responsible for polyploidization and megakaryocyte (MK) maturation. The Cip/Kip family of cyclin-dependent kinase (CDK) inhibitors which include p21Cip1 , p27Kip1 and p57Kip2 plays a crucial role in coupling cell-cycle arrest with differentiation in many cell types. MKs express high levels of p21Cip1 and p27Kip1 during differentiation. We hypothesized that these proteins act redundantly to arrest endomitosis and to induce terminal differentiation. We showed that only p21Cip1 was probably responsible for the arrest of endomitotic cell cycles by studying megakaryocytopoiesis of mice lacking one or the two proteins and the effects of overexpression of these proteins on megakaryocytopoiesis. Nevertheless, this murine model is insufficient to affirm thé absence of functional redundance between p21Cip1 and p27Kip1 during MK differentiation. We next showed the mammalian Target Of Rapamycin (mTOR) stimulation by TPO in MKs. This cell signaling pathway regulates cell growth (cell mass and cell size) of many cell types by increasing G1 phase progression through the TORC1 complex. We studied the rapamycin effects on culture of primary MKs and showed that mTOR pathway regulates MK proliferation, ploidization and size by increasing cyclin D3 and p21Cip1 transcription. In addition, mTOR régulates proplatelet formation independently from its effects on ploidization and cell growth
Hannou, Sarah Anissa. "Rôle du régulateur du cycle cellulaire p16INK4a dans le développement du diabète de type 2 et dans les maladies métaboliques du foie gras ou NAFLD (Non-Alcoholic Fatty Liver Disease) : rôle de p16INK4a dans le contrôle de la néoglucogenèse hépatique et dans le développement de la stéatose hépatique non alcoolique." Thesis, Lille 2, 2014. http://www.theses.fr/2014LIL2S012/document.
P16INK4a is a tumor suppressor protein well described as a cell cycle regulator. p16INK4a blocks cyclin D/ cyclin dependent kinase (CDK) 4 activity by binding to the catalytic subunit of CDK4, preventing retinoblastoma protein phosphorylation and subsequently the release of the E2F1 transcription factor. As a consequence; the transcription of genes required for progression to the S phase is restrained. Recently, genome-wide association studies (GWAS) associated the CDKN2A locus, encoding, amongst other genes, p16INK4A, with an increased risk of type 2 diabetes (T2D) development. However, the pathophysiological link between p16INK4a and hepatic glucose homeostasis remains unknown. In this context, we investigated the role of p16INK4a in hepatic glucose metabolism in vivo using p16+/+ and p16-/- mice and in vitro using primary hepatocytes and the AML12 hepatocyte cell line.p16-/- mice exhibited a higher response to fasting as shown by an increased hepatic gluconeogenic gene expression including phosphoenolpyruvate carboxykinase (PEPCK), fructose-1,6-biphosphatase (F1,6P) and glucose-6-phosphatase (G6Pase). p16-/- mice displayed an enhanced hepatic gluconeogenic activity in vivo upon administration of pyruvate, a gluconeogenic substrate. Consistent with this, in vitro data show that p16-/- primary hepatocytes display an enhanced gluconeogenic response to glucagon. In addition, knock down of p16INK4a by siRNA in AML12 cells increased gluconeogenic gene expression. These effects were associated with an increased activity of the PKA-CREB signaling pathway which leads to increased PPARg coactivator 1 (PGC1)α expression, a key transcriptional co-activator that regulates genes involved in energy metabolism. These findings describe a new function for p16INK4a as an actor in the hepatic adaptation to metabolic stress and suggest that p16INK4a could play a role during T2D development
Bramsiepe, Jonathan. "A function of cell-cycle regulation in pattern formation : endoreplication controls cell-fate maintenance in Arabidopsis." Thesis, Strasbourg, 2013. http://www.theses.fr/2013STRAJ119.
Cell differentiation is often linked with a switch from a mitotic to an endoreplication cycle, in which cells re-replicate their DNA without cell division. The molecular regulation of endoreplication and its biological fonction are only poorly understood. Here, I have used trichomes (leaf hairs) of Arabidopsis as a model to study cell differentiation and endoreplication. My work revealed that endoreplication cycles in Arabidopsis are controlled by cyclin dependent kinase (CDK) inhibitor proteins, which in turn are subject to protein degradation mediated by the action of SKP-CULLIN-F-BOX (SCF) complexes. This presumably creates oscillating levels of CDK activity, which are needed for repeated progression through DNA synthesis phases in endoreplicating cells. However, overexpression of CDK inhibitors did not only block endoreplication but also resulted in the dedifferentiation of trichome precursor cells. Similar observations were made with weak- loss-of-function alleles for the major CDK in Arabidopsis, CDKA;1, giving rise to the notion that endoreplication is required for cell fate maintenance. Trichome dedifferentiation was enhanced when trichome fate regulators were mutated. Surprisingly, the dedifferentiation could be at least partially repressed when RBR1, the Arabidopsis homolog of the animal tumor suppressor protein Retinoblastoma (Rb), was concomitantly mutated. Similarly, a mutation in PRCZ-methyltransfcrase CURLY LEAF (CLF) rescued the trichome maintenance defect of weak CDKA;1 mutants. Taken together, this suggests that PRC2 and RBR1 set a dynamic tissue threshold for cell differentiation during epidermis development in Arabidopsis
Kanjo, Ghaidaa. "Influence de Toxoplasma Gondii dans la régulation d'UHRF1 via la voie NF-KB." Thesis, Strasbourg, 2014. http://www.theses.fr/2014STRAJ068/document.
T.gondii interferes with the activation of NF-kB signaling pathways. Thus, upon infection by T.gondii, 85% of genes NF-kB-dependent are up-regulated. Another transcription factor whose expression is modulated by the parasite is UHRF1 (Ubiquitin-like, Containing PHD and RINGfinger domains, 1). UHRF1, bind to the gene promoter of cyclin b and induces epigenetic repression of this gene leading to cell cycle arrest in G2 phase of infected cells and stop the proliferation in both infected cells and parasite. In silico analysis of the uhrf1 gene promoter has been shown to possess 9 binding sites of NF-kB. Our study showed that NF-kB actually interacts with the promoter of gene uhrf1 during infection with T. gondii. This suggests that the expression of UHRF1 is modulated by NF-kB in T. gondii-infected cells. In addition we observed differential regulation of UHRF1 depending on the nature of the infecting strain. These variations may also be due to already well-known differential regulation of NF-kB by different strains of T.gondii. Determining the precise role of UHRF1 activation in infected cells and the identification of the parasitic factor responsible of this activation would allow to a better understanding of the mechanisms of intracellular persistence of the parasite and allow to unravel new therapeutic trails
Achour, Lamia. "Contrôle de l'expression à la surface cellulaire du récepteur de chimiokine CCR5." Paris 5, 2009. http://www.theses.fr/2009PA05T011.
CCR5 a chemokine receptor belonging to the G protein-coupled receptor (GPCR) family, plays a major role in HIV entry, by forming the viral receptor in association with the glycoprotein CD4. We report that the vast majority of fully functional CCR5 (=90%) is maintained within the intracellular compartments of human immune cells and of transfected fibroblasts. Intracellular CCR5 is mostly localized in the endoplasmic reticulum (ER) and the Golgi apparatus. The molecular mechanisms which control the export of CCR5 from the intracellular compartments are different in the ER and the Golgi. In the ER, the progression of CCR5 is slow and depends on its association with CD4 which functions as an escort protein and controls the CCR5 exit. Association with CD4 would induce a conformational change of CCR5, which would release the receptor from its retention in the ER by a resident protein, PRAF2. In the Golgi, the release of CCR5 is faster (5-10min) and is controlled by extracellular signals promoted by cell adhesion. The intracellular retention of CCR5 and, more generally, of GPCRs could represent an adaptive mechanism to maintain a prolonged physiological response. In particular contexts, which require sustained receptor response such as leukocyte chemotaxis, intracellular receptors would allow the permanent replacement of cell surface desensitized and internalized receptors