Letteratura scientifica selezionata sul tema "Brin d’ADN"
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Articoli di riviste sul tema "Brin d’ADN"
Depei, Liu. "Les techniques de génie génétique par recombinaison des oligonucléotides sur un seul brin d’ADN (SSOMR)". Bulletin de l'Académie Nationale de Médecine 188, n. 3 (marzo 2004): 471. http://dx.doi.org/10.1016/s0001-4079(19)33776-8.
Testo completoOudira, H., D. Djamai e A. Saifi. "Application d’un modèle déterministe à l’étude de l’influence des molécules radioprotectrices sur les rendements des cassures simple et double brin de la molécule d’ADN". Radioprotection 43, n. 3 (luglio 2008): 389–408. http://dx.doi.org/10.1051/radiopro:2008006.
Testo completoLestienne, Patrick. "Trois brins d’ADN dans le centre catalytique des ADN polymérases". médecine/sciences 20, n. 10 (ottobre 2004): 854–56. http://dx.doi.org/10.1051/medsci/20042010854.
Testo completoPoulichet, P., L. Rousseau, J. Pagazani e O. Français. "Lab-On-a-Chip : réalisation d'une PCR “Polymerase Chain Reaction”". J3eA 21 (2022): 1021. http://dx.doi.org/10.1051/j3ea/20221021.
Testo completoBaba, S. S. "Détection de l'ARN et de l'antigène du virus de la rage dans des tissus de chiens infectés naturellement au Nigeria : hybridation in situ et études immunohistochimiques". Revue d’élevage et de médecine vétérinaire des pays tropicaux 52, n. 2 (1 febbraio 1999): 85–91. http://dx.doi.org/10.19182/remvt.9691.
Testo completoGagné, François, Christian Blaise, Jocelyne Pellerin e Michel Fournier. "Études de biomarqueurs chez la mye commune (Mya arenaria) du fjord du Saguenay : bilan de recherches (1997 à 2006)". 22, n. 2 (15 giugno 2009): 253–69. http://dx.doi.org/10.7202/037484ar.
Testo completoTesi sul tema "Brin d’ADN"
Fiston-Lavier, Anna-Sophie. "Etude de la dynamique des répétitions dans les génomes eucaryotes : de leur formation à leur élimination". Paris 6, 2008. https://tel.archives-ouvertes.fr/tel-00283414.
Testo completoAmarir-Bouhram, Jihane. "Évolution des génomes de bactériophages". Phd thesis, Université Paris Sud - Paris XI, 2012. http://tel.archives-ouvertes.fr/tel-00923139.
Testo completoHachin, Axelle. "Développement d'une plateforme de détection SERS à partir de monocouches auto-assemblées". Electronic Thesis or Diss., Bordeaux, 2023. http://www.theses.fr/2023BORD0481.
Testo completoBiosensors are real-time detection systems for biological species widely used in diagnostics. Surface Enhanced Raman Spectroscopy (SERS), with its specific and sensitive identification capability, is a good way of detecting biomolecules (aptamers, peptides, etc.) using suitable surfaces (such as metal nanostructures, nanoparticles, etc.). With a view to developing a SERS biosensor, a detection platform based on self-assembled monolayers (SAMs) functionalized with spherical or cylindrical gold nanoparticles was designed. The thesis work consisted in producing SAMs based on organosilane bearing an azide or amine terminal function. The SAMs were then modified by reaction with linkers, either by peptide coupling or click chemistry, to provide thiol or cyclooctyne end functions. These modifications are characterized by various techniques such as PM-IRRAS, AFM, XPS or ToF-SIMS. Gold nanoparticles have been successfully immobilized by two different routes: on azide-terminated SAMs by click chemistry and on thiol-terminated SAMs by ligand exchange. Promising initial results have been obtained demonstrating SERS detection of the bioreceptor immobilized on the nanoparticles
Lowry, Carolyne Mary. "Alterations of the epigenome in brain cancer: loss of 5-hydroxymethylcytosine". Mémoire, Université de Sherbrooke, 2017. http://hdl.handle.net/11143/9864.
Testo completoRésumé : 5Mtéthylcytosine (5mC) est une marque épigénétique qui peut être oxydée en 5-hydroxyméthylcytosine (5hmC) par ten-eleven translocation (TET) oxygénases. Ceci amène à l’étape initiale de la déméthylation de 5mC. Le niveau de 5hmC est plus élevé dans le cerveau par rapport aux autres organes. Par contre, ce niveau a une réduction marquante au cours du développement d’une tumeur cérébrale, notamment le glioblastome multiforme (GBM). Toutefois, il n’y a aucun mécanisme connu pour expliquer cette anomalie. Les objectifs de ce projet étaient de (1) discerner l’implication de la voie de déméthylation obtenu par médiation de TET et (2) d’avoir une compréhension plus profonde de la constitution épigénétique des tumeurs cérébraux. (1) Des cellules U87 ont été incubées avec 5mC, 5hmC, 5-fomylcytosine (5fC) et une co-incubation de 5hmC avec 3,4,5,6-tétrahydro-2’-déoxyuridine (dTHU). Les échantillons ont été récoltés à 0, 24, 48, 96 heures. (2) 130 tumeurs cérébraux (GBM = 79; grade II/III = 51) étaient obtenus directement de chirurgie et mise en suspension dans un tampon d’extraction d’ADN le jour même. Les échantillons d’U87 et de tissu tumoral ont subi les protocoles d’extraction et de digestion d’ADN. Le pourcentage par cytosine (%/C) était calculé par la quantification de 5mC, 5hmC, 5fC, 5-hydroxyméthyluracile (5hmU) et 5-formyluracile (5fU) en utilisant LC-MS/MS. (1) Les incubations d’U87 ont démontrées la possibilité augmenter les niveaux génomique de 5hmC, mais aussi une légère augmentation des niveaux de 5mC. Les niveaux de 5hmC ont accru de 1.9 fois après 96hrs. Par contre, aucune variation n’a été observée dans les niveaux de 5fC. Les incubations de 5hmC et 5fC ont été accompagnées par une élévation des niveaux de 5hmU et 5fU respectivement. L’addition de dTHU avec 5hmC avait diminué l’incorporation de 5hmU par 65%. (2) Dans les tumeurs cérébraux, les niveaux moyens de 5mC, 5hmC et 5fC étaient de 4.0, 0.15 et 0.021%/C respectivement. Les quantités de 5hmU et 5fU étaient grandement plus faible dans le GBMs que dans les tumeurs de bas grades. La présence de 5hmU et 5fU dans les tumeurs et leur augmentation durant l’incubation des U87 indiquent une activité de désamination, qui peut, en particulier, entraver les niveaux de 5hmC. En outre, malgré l’incubation avec 5mC, les niveaux de 5hmC et 5fC n’ont pas augmentés suggérant un dysfonctionnement de TET. L’activité de TET est maintenue dans GBM, mais altérée dans les tumeurs de bas grades à cause de mutation isocitrate dehydrogenase-1 (IDH1). Par conséquent, la forte activité de désamination et la déficience en TET peuvent conduire à une réduction épigénétique.
Yu, Helen. "Caractérisation fonctionnelle du suppresseur de tumeurs BAP1". Thèse, 2015. http://hdl.handle.net/1866/12094.
Testo completoThe deubiquitinase BAP1 (BRCA1-Associated Protein1) is a nuclear member of the ubiquitin C-terminal hydrolase (UCH) family, previously isolated for promoting the function of the tumor suppressor BRCA1. Importantly, homozygous inactivating mutations of BAP1 have been found in mesothelioma, renal, melanoma and breast cancers strongly suggesting that this deubiquitinase is a tumor suppressor. Indeed BAP1 overexpression reduces cell proliferation and tumor growth in xenograft models. Nonetheless, the biological function and the mechanism of action of this deubiquitinase remain poorly defined. The goals of this thesis are to characterize the biological function of BAP1 and to reveal the molecular basis of its tumor suppressive function. To provide insights into BAP1 biological function, we conducted a tandem affinity immunopurification of BAP1-associated proteins and found that most interacting partners are transcription factors and cofactors. Next, we demonstrated that BAP1 is indeed a transcription regulator. Concomitantly, another group showed that the drosophila BAP1, Calypso, is a Polycomb Group protein that regulates the ubiquitination levels of H2A and gene expression. Indeed, our global gene expression analysis suggests that BAP1 plays important role in DNA damage response. Consistently, loss- and gain- of function experiments (RNAi approach, DT40 chicken B cells KO model and re-introduction of BAP1 in BAP1 null-cells) revealed that BAP1 promotes homologous recombination-mediated DNA double strand break repair. Our data suggest that BAP1 exerts its tumor suppressor function by controlling error-free DNA repair by homologous recombination. Thus, in a situation of BAP1 inactivation, cells might become more reliant on non-homologous end joining, an error-prone DNA repair mechanism, which would result in the accumulation of mutations and chromosomal aberrations, causing genomic instability. Further studies are required to delineate the exact role of BAP1 in transcription and to define how deregulation of H2A ubiquitination pathway contributes to cancer. Defining the mechanisms of tumor suppression is of great interest, not only for understanding cancer development, but also for designing rational cancer therapies.
Alecki, Célia. "L’identification de nouvelles activités chez les complexes Polycomb les lient aux structures d’ADN non-canoniques". Thesis, 2020. http://hdl.handle.net/1866/24575.
Testo completoPolycomb group (PcG) proteins are conserved, essential proteins, which assemble in two main complexes, PRC1 and PRC2, which are targeted to chromatin and stably repress gene expression. In Drosophila melanogaster, Polycomb complexes are targeted to DNA elements called Polycomb response elements (PREs) to repress transcription. PREs are switchable memory elements that can maintain either gene repression or gene activation. Despite decades of study, fundamental questions about how the PcG system functions remain. These include: 1) how PcG proteins are targeted to PREs only in the appropriate developmental context, and how PREs can mediate both stable activation and repression; 2) how PcG complexes repress transcription, and whether it involves novel biochemical mechanisms and interactions; 3) how PcG repression can be propagated through cell cycles. The search for new biochemical activities for PcG complexes that may answer these questions is the topic of this thesis. PREs are transcribed into RNAs which may give the context specificity to recruit PcG proteins. We hypothesized that R-loops may form at PREs, and be recognized by PcG complexes, which we tested in Chapter 2. We identified R-loop forming sequences in Drosophila melanogaster embryos and tissue culture cells, and found that ~30% of the PREs form R-loops. We found that PREs which have formed R-loops are more likely to be bound by PcG proteins both in vivo and in vitro. PRC2 binds to thousand RNA in vivo but no clear activity has been associated with it. Using in vitro assays, we identified a strand exchange activity for PRC2 which induces the formation of RNA-DNA hybrid, the main part of an R-loop. In this chapter, we have found that PREs form R-loops and are involved in the targeting of PcG proteins which induce stable gene repression. We have discovered an RNA strand exchange activity for PRC2 which may involve this Polycomb complex in the formation of R-loops in vivo. In Chapter 3, we identified a type I topoisomerase-like activity associated with PRC1 and the C-terminal region of its subunit PSC (PSC-CTR). PRC1 and PSC-CTR can relax a negatively supercoiled plasmid and add negative coils to a relaxed plasmid in absence of topoisomerase. This activity suggests regulation of DNA topology may be a novel mechanism used by PcG complexes. PRC1 can resolve R-loops formed on negatively supercoiled DNA in vitro. One role for the topoisomerase-like activity may be to regulate R-loops, whose stability of depends on both the DNA sequence and the topology of the surrounding DNA, in vivo. In this thesis, we identified new activities for Polycomb group complexes: an RNA strand exchange activity for PRC2 and a topoisomerase-like activity for PRC1. Both activities link PcG complexes to the formation and resolution of R-loops. In addition, both complexes can recognize R-loops and are recruited to PREs which have formed these structures. In conclusion, we have identified new nucleic acid-based activities for the Polycomb complexes PRC1 and PRC2, which link them to the formation, recognition and resolution of R-loops.
Capitoli di libri sul tema "Brin d’ADN"
FEARNS, Rachel. "Virus à ARN brin négatif". In Virologie, 73–105. ISTE Group, 2022. http://dx.doi.org/10.51926/iste.9023.ch3.
Testo completo