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Artykuły w czasopismach na temat "Réparation de l'ADN mitochondrial"
Kahn, A. "Ubiquitine, cycle cellulaire et réparation de l'ADN". médecine/sciences 4, nr 1 (1988): 59. http://dx.doi.org/10.4267/10608/3753.
Pełny tekst źródłaBoorstein, R., J. Cadet, LN Chiu, S. Zuo i G. Teebor. "Réparation des modifications oxydatives de l'ADN : cas de la 5-méthylcytosine dans l'ADN". Journal de Chimie Physique 91 (1994): 984–94. http://dx.doi.org/10.1051/jcp/1994910984.
Pełny tekst źródłaSarasin, A. "Les gènes humains de la réparation de l'ADN". médecine/sciences 10, nr 1 (1994): 43. http://dx.doi.org/10.4267/10608/2479.
Pełny tekst źródłaPourquier, Philippe, i Jacques Robert. "Présentation générale des mécanismes de réparation de l'ADN". Bulletin du Cancer 98, nr 3 (marzec 2011): 229–37. http://dx.doi.org/10.1684/bdc.2011.1323.
Pełny tekst źródłaBoiteux, S., i JP Radicella. "Réparation de l'ADN et cancer : Les gènes de réparation des bases oxydées dans l'ADN sont-ils des gènes suppresseurs de tumeurs ?" médecine/sciences 14, nr 3 (1998): 310. http://dx.doi.org/10.4267/10608/1034.
Pełny tekst źródłaBoorstein, RJ, J. Cadet, T. Hilbert, M. Lustig, R. O'Donnell, S. Zuo i G. Teebor. "Formation, stabilité et réparation de modifications pyrimidiniques dans l'ADN". Journal de Chimie Physique 90 (1993): 837–52. http://dx.doi.org/10.1051/jcp/1993900837.
Pełny tekst źródłaFeunteun, J. "BRCA1 et BRCA2 : des échafaudages de réparation des lésions de l'ADN ?" médecine/sciences 17, nr 10 (2001): 1070. http://dx.doi.org/10.4267/10608/1824.
Pełny tekst źródłade MURCIA, Gilbert, Miguel MOLINETE, Valérie SCHREIBER, Frédéric SIMONIN, Gérard GRADWOHL, Claude NIEDERGANG, Muriel MASSON i Josiane MÉNISSIER-de MURCIA. "Poly (ADP-ribosyl) ation et réparation de l'ADN chez les eucaryotes". Radioprotection 28, nr 1 (styczeń 1993): 57–61. http://dx.doi.org/10.1051/radiopro/1993031.
Pełny tekst źródłaSchaeffer, L., i JM Egly. "BTF2/TFIIH, un facteur de transcription et réparation impliqué dans des maladies de la réparation de l'ADN". médecine/sciences 10, nr 10 (1994): 973. http://dx.doi.org/10.4267/10608/2503.
Pełny tekst źródłaSarasin, A. "La réparation de l'ADN au centre de la biologie de la cellule". médecine/sciences 10, nr 10 (1994): 951. http://dx.doi.org/10.4267/10608/2499.
Pełny tekst źródłaRozprawy doktorskie na temat "Réparation de l'ADN mitochondrial"
Wallet, Clementine. "L'hélicase RECG1, un facteur-clé dans le maintien et la ségrégation de l'ADN mitochondrial d'Arabidopsis thaliana". Thesis, Strasbourg, 2016. http://www.theses.fr/2016STRAJ016/document.
Pełny tekst źródłaThe mitochondrial DNA (mtDNA) of flowering plants is characterized by the recombination activities that modulate its structure. These activities are required for the mtDNA maintenance, and drive its rapid structural evolution. The factors that control recombination are therefore essential for plant mtDNA stability. During my PhD, I identified and characterized two DNA helicases that are present in the organelles of Arabidopsisthaliana. One is the homologue of a bacterial helicase involved in transcription-coupled repair. Its role in the plant organelles is still not determined. The other one, the RECG1 helicase, has roles in recombination dependent repair, the surveillance of ectopic recombination involving short repeated sequences, and also the segregation of the mtDNA. We have found that in the absence of RECG1 there is loss of recombination control resulting in the occurrence of alternative versions of the mtDNA generated by recombination. The analysis oftheir segregation, induced by RECG1, allowed us to build a model to how new stable mtDNA configurations are generated by the stoichiometric shift of mtDNA sub-genomes. This work allowed us to better understand the recombination and segregation mechanisms that modulate the Arabidopsis mtDNA
Kubilinskas, Rokas. "MitoTALENs to explore mitochondrial DNA repair and segregation". Electronic Thesis or Diss., Strasbourg, 2024. http://www.theses.fr/2024STRAJ014.
Pełny tekst źródłaFor long, the plant mitochondrial genome (mtDNA) was not amenable to manipulation, until recent advancements in genome engineering using Transcription Activator-Like Effector Nucleases (TALEN). In this work I used TALENs specifically targeted to mitochondria (mitoTALENs) to study plant mtDNA repair and segregation. MitoTALEN constructs were transformed into the background of 10 different Arabidopsis thaliana mutant lines, deficient in various factors involved in plant mitochondrial repair by homologous recombination. The resulting lines were analysed by Illumina sequencing and qPCR approaches. In wild type plants, the mtDNA double-strand-break (DSB) induced by MitoTALENs was repaired by homologous recombination, resulting in the replacement of the region containing the DSB by a distal unaffected sequence of the mtDNA, flanked by the same set of repeated sequences. In mutants deficient in repair factors, repair could shift to alternative pathways, such as Single-Strand Annealing (SSA) and Microhomology-mediated recombination (MHMR). Furthermore, in some mutants, the data revealed no evidence of DSB repair, but rather suggested that plants deficient in key repair factors could survive by reconstituting an alternative viable mitochondrial genome, from pre-existing autonomously replicating sub-genomes
Moretton, Amandine. "Mécanismes de maintenance de l'intégrité de l'ADN mitochondrial humain suite à des cassures double-brin". Thesis, Université Clermont Auvergne (2017-2020), 2017. http://www.theses.fr/2017CLFAC047/document.
Pełny tekst źródłaMitochondria are organelles that possess their own genome, the mitochondrial DNA (mtDNA). Repair of oxidative damages, defective replication, or various exogenous sources, such as chemotherapeutic agents or ionizing radiations, can generate double-strand breaks (DSBs) in mtDNA. MtDNA encodes for essential proteins involved in ATP production and maintenance of integrity of this genome is thus of crucial importance. Mutations in mtDNA are indeed found in numerous pathologies such as mitochondrial myopathies, neurodegenerative disorders or cancers. However, the mechanisms involved in mtDNA maintenance after DSBs remain unknown.To elucidate this question, we have generated mtDNA DSBs using a human inducible cell system expressing the restriction enzyme PstI targeted to mitochondria. Using this system, we could not find any support for DSBs repair of mtDNA. Instead we observed a loss of the damaged mtDNA molecules and a severe decrease in mtDNA content, followed by reamplification of intact mtDNA molecules. We have demonstrated that none of the known mitochondrial nucleases are involved in mtDNA degradation and that DNA loss is not due to autophagy, mitophagy or apoptosis but to a selective mechanism. Our study suggests that a still uncharacterized pathway for the targeted degradation of damaged mtDNA in a mitophagy/autophagy-independent manner is present in mitochondria, and might provide the main mechanism used by the cells to deal with DSBs. Global approaches are ongoing to identify proteins involved in degradation of damaged mtDNA following DSBs, mainly an RNAi screen targeting 80 nucleases. In parallel we are interested in a family of phosphohydrolases named Nudix and their putative protective role in sanitizing the nucleotides pool in mitochondria
Martinet, Pervenche. "Peau et anomalies de la réparation de l'ADN aux ultraviolets : à propos d'une observation associant dyschromie, syndrome cérébelleux et dysfonctionnement mitochondrial". Aix-Marseille 2, 1994. http://www.theses.fr/1994AIX20831.
Pełny tekst źródłaIqbal, Rana khalid. "Approches biotechnologiques de l'expression et de la diversité du génome mitochondrial des plantes". Thesis, Strasbourg, 2017. http://www.theses.fr/2017STRAJ035/document.
Pełny tekst źródłaThe mitochondrial DNA of plants is dynamic and its expression is complex. Using a strategy based on the natural import of nuclear-encoded transfer RNAs from the cytosol, we targeted to mitochondria in Arabidopsis thaliana the orf77 RNA characteristic for S-CMS in maize and we analyzed the effects on the transcriptome. The results showed that the mitochondrial transcriptome is tighly regulated during plant development and is strongly buffered at early stages. Mitochondrial targeting of orf77 also triggered a cross-talk with the nucleus. On the other hand, DNA replication and repair in plant mitochondria involve active recombination controled by nuclear-encoded factors. We identified a new member of this set of factors, the 5'-3' exonuclease potentially responsible for the resection of DNA ends in recombination-mediated repair of double-strand breaks. As a whole, the results open prospects for generating mitochondrial genetic diversity and creating CMS lines with agronomical interest
Boesch, Pierre. "Caractérisation d'un mécanisme de réparation de l'ADN par excision de base dans les mitochondries des cellules végétales". Université Louis Pasteur (Strasbourg) (1971-2008), 2005. http://www.theses.fr/2005STR13181.
Pełny tekst źródłaMitochondria possess their own DNA (mtDNA) and are a major source for Reactive Oxygen Species (ROS) production. Due to its close proximity to the ROS source the mtDNA is a likely to be oxidized. 8-oxo-guanine (8oxoG) and uracile are the most studied oxidative lesion and are repaired by the Base Excision Repair (BER) pathway. This DNA repair pathway is also the only one found with absolute certainty in mitochondria. As the question of DNA repair in plant’s organelles remains open our laboratory has initiated a study whose aim was to show whether mitochondria and chloroplast are able to repair DNA or not. In a first set of in vitro experiments we have shown that plant organelle do actually harbor DNA glycosylase and AP endonuclease activities, and that some part of each activities is somehow present in a membrane associated fashion. The second set of in organello experiments has enable us to show that a DNA carrying uracile can be imported and fully repaired in plant mitochondria. So, these organelles do actually have also DNA repair synthesis and ligase activity. The presence of a complete BER pathway in plant mitochondria is thus undoubtful, but the question of its association with the membrane remains open and the protein involved in this pathway should still be identified
Rageul, Julie. "Rôles d'ERCC1, une protéine clé de la réparation de l'ADN, dans la progression du cycle cellulaire et la survie des cellules humaines, tumorales ou non". Rennes 1, 2011. http://www.theses.fr/2011REN1B081.
Pełny tekst źródłaERCC1-XPF (Excision Repair Cross Complementing gene 1/Xeroderma Pigmentosum group F) is a heterodimeric endonuclease involved in many DNA repair systems. Phenotypes of ERCC1 deficiency in diverse organisms suggest that this protein may have an additional role in the regulation of cell cycle progression. To evaluate this hypothesis in human tumoral and non-tumoral cell lines, we knocked-down ERCC1 by RNA interference (ERCC1KD). Our results have shown that ERCC1KD cells become multinucleated, not only in tumoral cells but also in non-tumoral cells and regardless of tissue type. These multinucleated cells accumulate nuclei through abnormal mitoses ending by a defective cytokinesis. In addition, when mitotic abnormalities are too drastic, ERCC1KD cells die in mitosis, and this is highly reminiscent of mitotic catastrophe. In an original way, cells knocked-down for XPF do not share this phenotype of multinucleation, suggesting for the first time that ERCC1 could bear a new role, independently of its known DNA repair activity. Furthermore, we have provided evidence suggesting that this new role of ERCC1 could potentially involve the oxidant/antioxidant balance and could be linked to a mitochondrial function. This ERCC1 new role may be crucial for development, growth, proliferation and cell survival. Finally, it may be conceivable that ERCC1 might become a new promising therapeutic target for cancer treatment
Paraf, François. "Gènes de réparation de l'ADN et Cancers Colorectaux". Université de Limoges. Faculté de médecine et de pharmacie, 2001. http://www.theses.fr/2001LIMO102B.
Pełny tekst źródłaEot-Houllier, Grégory. "Réparation in vitro de sites multilésés de l'ADN". Paris 11, 2005. http://www.theses.fr/2005PA11T018.
Pełny tekst źródłaJobin-Robitaille, Olivier. "Dynamique chromatinienne dans la réparation de l'ADN : analyse fonctionnelle du complexe histone acétyltransférase NuA4 dans la réparation des dommages à l'ADN". Thesis, Université Laval, 2005. http://www.theses.ulaval.ca/2005/22935/22935.pdf.
Pełny tekst źródłaInscrit au Tableau d'honneur de la Faculté des études supérieures
Książki na temat "Réparation de l'ADN mitochondrial"
Alain, Branchaud, red. Identification des larves et des oeufs des suceurs, Moxostama, par analyse de l'ADN mitochondrial. Québec: Gouvernement du Québec, Ministère de l'environnement et de la faune, Direction de la faune et des habitats, 1996.
Znajdź pełny tekst źródłaA, Nickoloff Jac, i Hoekstra Merl F, red. DNA damage and repair. Totowa, N.J: Humana Press, 1998.
Znajdź pełny tekst źródłaBernatchez, Louis. Comparaison de l'ADN mitochondrial des éperlans arc-en-ciel (Osmerus mordax) frayant dans les régions de Beaumont, de Rivière-Ouelle et de la Baie des Chaleurs en 1990. Québec: Ministère du loisir, de la chasse et de la pêche, 1992.
Znajdź pełny tekst źródłaEssai n° 482: Toxicologie génétique: Lésion et réparation d'ADN - Synthèse non programmée de l'ADN (UDS) sur cellules de mammifère - in vitro. OECD, 1986. http://dx.doi.org/10.1787/9789264071452-fr.
Pełny tekst źródłaDNA Damage and Repair: Volume II: DNA Repair in Higher Eukaryotes (Contemporary Cancer Research). Humana Press, 1998.
Znajdź pełny tekst źródła(Editor), Jac A. Nickoloff, i Merl F. Hoekstra (Editor), red. DNA Damage and Repair: Volume I: DNA Repair in Prokaryotes and Lower Eukaryotes (Contemporary Cancer Research). Humana Press, 1998.
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