Academic literature on the topic 'Mécanisme de transcription'
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Journal articles on the topic "Mécanisme de transcription":
Martella, Christophe, Laetitia Waast, and Claudine Pique. "Tax, marionnettiste de la transcription du HTLV-1." médecine/sciences 38, no. 4 (April 2022): 359–65. http://dx.doi.org/10.1051/medsci/2022039.
Lacazette, Éric, Leila Halidou Diallo, Florence Tatin, Barbara Garmy-Susini, and Anne-Catherine Prats. "L’ARN circulaire nous joue-t-il des tours ?" médecine/sciences 36, no. 1 (January 2020): 38–43. http://dx.doi.org/10.1051/medsci/2019267.
Ricquebourg, Rebekah, and Nikolaos Konstantinides. "Un mécanisme temporel pour la génération de la diversité neuronale." médecine/sciences 40, no. 3 (March 2024): 251–57. http://dx.doi.org/10.1051/medsci/2024012.
Arellano-Soto, German, and Susan Parks. "The Role of Multimodality during the Negotiation of Meaning in an English/Spanish eTandem Video-Conferencing Exchange." Canadian Modern Language Review 77, no. 2 (May 2021): 129–53. http://dx.doi.org/10.3138/cmlr-2019-0030.
Briand, P. "Transcription illégitime : implications et mécanismes possibles." médecine/sciences 6, no. 1 (1990): 55. http://dx.doi.org/10.4267/10608/4062.
Dassa-Valzer, Manon, Romain Debiton, Margaux Gibert, Alexandre Lutz, and Amel Latifi. "Diversité des mécanismes de transcription des virus géants." médecine/sciences 36, no. 4 (April 2020): 412–15. http://dx.doi.org/10.1051/medsci/2020066.
Rey, R., S. Ragot, J. C. Chauvet-Gelinier, B. Bonin, and J. R. Teyssier. "Surexpression des gènes impliqués dans les mécanismes épigénétiques réprimant la transcription dans le cortex cérébral et les leucocytes sanguins des patients dépressifs." European Psychiatry 30, S2 (November 2015): S118—S119. http://dx.doi.org/10.1016/j.eurpsy.2015.09.227.
Furlan, Alessandro, Florence Agbazahou, Mélanie Henry, Mariano Gonzalez-Pisfil, Corentin Le Nézet, Dorian Champelovier, Marie Fournier, Bernard Vandenbunder, Gabriel Bidaux, and Laurent Héliot. "P-TEFb et Brd4." médecine/sciences 34, no. 8-9 (August 2018): 685–92. http://dx.doi.org/10.1051/medsci/20183408015.
Peyron, JF, and A. Livolsi. "Dissection moléculaire des mécanismes d'activation du facteur de transcription NF-κB : de nouvelles cibles thérapeutiques en prévision." médecine/sciences 15, no. 3 (1999): 419. http://dx.doi.org/10.4267/10608/1359.
Filhoulaud, G., J. Girard, and C. Postic. "P203 - La O-GlcNAcylation du facteur de transcription ChREBP contribue aux mécanismes de glucotoxicité dans la cellule bêta pancréatique." Diabetes & Metabolism 37, no. 1 (March 2011): A81—A82. http://dx.doi.org/10.1016/s1262-3636(11)70829-1.
Dissertations / Theses on the topic "Mécanisme de transcription":
Tremblay, Jacques. "Mécanisme d'action de PTX1, un facteur de transcription à homéodomaine." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/nq43040.pdf.
Flajollet, Sébastien. "Etude du mécanisme d'activation de la transcription en réponse aux rétinoïdes." Lille 2, 2006. http://www.theses.fr/2006LIL2S041.
The Retinoic Acid Receptor (RAR) is a ligand activated transcription factor which modulates the expression of retinoic acid-target genes. These genes are implied in fundamental biological processes such as cellular homeostasis, embryogenesis, growth and reproduction. RAR recruits a plethora of coregulators with multiple functions in response to retinoids. These multiprotein complexes are key structural components in the complex and controlled transcription mechanism. Many of them participate in remodeling of chromatin, while otehrs are implied transcription complex formation. This underlines the importance of these coactivators in transcriptional activation. Yet their contribution to RAR-mediated transactivation remains poorly studied. This PhD thesis focused on the recruitment of three coactivator complexes : P160, mediator and SWI/SNF complex. These proteins are implied in distinct steps of the RAR-mediated process. I investigated this question by assessing the respective role of these coactivators by using molecular and cellular biology approaches in the P19 embryonal carcinoma cell line, an appropriate developmental system to study the role of RARs. Results of knock-down of SRC1 and med1 by RNA interference have demonstrated distinct roles of these coactivator complexes in retinoid-induced biological responses. This allowed us to propose a model summarizing complex formation during transcription initiation at the RARBeta2 promoter, a prototypical retinoic acid-regulated gene. Finally the study of the interaction between the ATP-dependent chromatin remodeling SWI-SNF complex and RAR identified us an additional step in the regulation of transcription by retinoids. Characterization of the role of each coactivators provide important information to better understand this complex regulation of RA-induced transcription
Tupin, Audrey. "Inhibiteurs de la transcription bactérienne : étude du mécanisme d'action de la lipiarmycine et dépendance au facteur de transcription σ." Thesis, Montpellier 1, 2010. http://www.theses.fr/2010MON13512/document.
The growing number of antibiotic-resistant bacteria added to the problem caused by persistent cells stress the need for developing new antibiotics and for understanding their mechanism of action. RNA polymerase is the main enzyme of the transcription process and is an interesting target for antibiotics. In this study we focus on a particular inhibitor of RNA polymerase : lipiarmycin. It is a macrocyclic inhibitor of transcription inhibiting Gram + bacteria that is developed in phase III clinical trials for treatment of Clostridium difficile infections. The objective of this work was to determine the mechanism of action of lipiarmycin and the mechanism confering resistance against the molecule. We first define more precisely its binding site on RNA polymerase and then used genetic and biochemical approaches to determine its mechanism of action and the effect of some specific mutations on transcription. Our experiments reveal a new mechanism of t ranscription inhibitor action
Moumen, Abdeladim. "Etude du mécanisme de la recombinaison homologue chez les rétrovirus." Paris 11, 2002. http://www.theses.fr/2002PA112133.
Homologous recombination is one of the main factors generating genetic variability in retrovirus. Recombination results from a transfer, by the reverse transcriptase, of the DNA synthesis from a genomic RNA (donor RNA) to the other one (acceptor RNA) presents within the virion. In order to dissect the molecular mechanism of this phenomenon, we have developed a reconstituted in vitro system, which allowed us to study recombination on any retroviral sequence of interest. One third of the genome has been investigated and most regions analysed yielded a high degree of recombination. We have identified, for the first time, that recombination efficiency of a given sequence was dependent on its folding and namely on the presence of a stable hairpin. This hairpin structure was required to be present in the acceptor RNA. Furthermore, we have shown that the strand transfer reaction is an intramolecular process where the acceptor RNA is complexed to the nascent DNA before the transfer. Based on these results, we have proposed a model of recombination in which the acceptor RNA, by its hairpin structure, hybridises to the nascent DNA before the switch occurs. This hybridisation both allows the acceptor RNA to be in close proximity with the nascent DNA and disrupts the process of reverse transcription ongoing on the donor RNA, thereby leading to a displacement of the donor RNA from the polemerase active site and its replacement by the acceptor RNA. It is well known that the folding of the RNA is involved in several biological processes, we have now demonstrated that it is also involved in the process, which generates genetic variability in retrovirus: homologous recombination
Debaize, Lydie. "Nouveau mécanisme d’activation d’un oncogène impliquant RUNX1 et FUBP1 dans les leucémies aiguës lymphoblastiques." Thesis, Rennes 1, 2018. http://www.theses.fr/2018REN1B016/document.
Hematopoiesis is initiated from hematopoietic stem cells and results in the continuous and controlled production of mature blood cells. RUNX1 (Runt-related transcription factor 1) encodes a transcription factor playing a key role in hematopoiesis. Abnormal functions of this protein are implicated in blood cancer, notably in pediatric B-cell precursor acute lymphoblastic leukemia (BCP-ALL). Moreover, its transcriptional activity is controlled by the recruitment of cofactors. To unravel the mechanisms behind the regulation of RUNX1 transcriptional activity, we performed RUNX1 specific immunoprecipitation experiments followed by mass spectrometry and identified the Far Upstream Element Binding Protein 1 (FUBP1) as a potential cofactor of RUNX1. FUBP1 is a multifunctional regulator involved in diverse cellular processes. FUBP1 has recently been described to be essential for expansion and self-renewal of hematopoietic stem cells and to function as a potential cancer driver gene in lymphoblastic leukemia. We have shown, with a proximity ligation assay that we have optimized in non-adherent cells, that FUBP1 is a new cofactor of RUNX1 and that these two proteins can be part of the same regulatory complex in human pre-B lymphoblasts. By chromatin immunoprecipitation combined with sequencing, we have localized common chromatin regions bound by RUNX1 and FUBP1. We have identified the oncogene c-KIT as a common target gene, and characterized two regulatory regions bound by both RUNX1, FUBP1 and active histone marks, within the first c-KIT intron: one at +700 bp and the other on an enhancer at +30 kb. Moreover, we have determined RUNX1 and FUBP1 binding sites essential for the enhancer activation. Finally, we have demonstrated that RUNX1 and FUBP1 overexpression in a pre-B cell line increases the expression of c-KIT both at mRNA and protein levels, exacerbates one of the c-KIT downstream pathways, promotes cell proliferation in vitro and in vivo and renders cells more resistant to a c-KIT inhibitor. In conclusion, we have demonstrated that FUBP1 is a new cofactor of RUNX1 and that they activate the transcription of the c-KIT oncogene by binding on a common enhancer, thus promoting cell proliferation. Therefore, since FUBP1 and RUNX1 are overexpressed in some types of leukemia, alterations in this regulation may contribute to the onset or maintenance of leukemias. These new findings open new perspectives on understanding the control of RUNX1 transcriptional activity, and on leukemias related to RUNX1, FUBP1 or c-KIT deregulations
Auriol, Jérôme. "Etude fonctionnelle du facteur de transcription/réparation TFIIH : rôles dans le mécanisme de réparation de l'ADN par excision de nucléotides." Université Louis Pasteur (Strasbourg) (1971-2008), 2002. http://www.theses.fr/2002STR13178.
TFIIH is a multiprotein complex involved in transcription of class II and class I genes, and in nucleotide excision repair (NER). The cellular importance of this complex is illustrated by genetic disorders associated with mutations in two subunits of TFIIH, the XPB and XPD helicases. Those helicases are essentials for transcriptional and DNA repair mechanisms. During my PhD studies, we became interested in the function of TFIIH in NER. We studied the molecular consequences of an XPB mutation which change the last 40 C-terminal amino acids. Mutation disrupts TFIIH activity both in transcription and in repair. This mutant allowed us to identify an XPB phosphorylation site required for the cellular functions of TFIIH. Moreover, we isolated a complex containing TFIIH, RNA polymerase I and two repair proteins XPG and CSB. This complex is involved in ribosomal RNA synthesis. We show that mutations within the CSB protein destabilized the complex. This is also true for mutations within XPB and XPD, arguing for the biological significance of this complex. Finally, in order to study the regulation of TFIIH expression, we study the organisation of murine gene coding for p62 subunit as well as its promoter
Caillier, Bertrand. "Mécanisme de régulation de la transcription de l'UGT1A3 au foie et effet de variants génétiques." Thesis, Université Laval, 2007. http://www.theses.ulaval.ca/2007/24528/24528.pdf.
Savare, Jean. "Mécanisme d'action du facteur de transcription SoxNeuro chez la drosophile : partenariat et modifications post-traductionnelles." Montpellier 1, 2005. http://www.theses.fr/2005MON13504.
Thénot, Sandrine. "Mécanisme d'activation de la transcription par les récepteurs aux oestrogènes : étude du cofacteur transcriptionnel hTIF1alpha." Montpellier 1, 2000. http://www.theses.fr/2000MON1T008.
Teyssier, Catherine. "Mécanisme de l'interférence transcriptionnelle entre le récepteur des oestrogènes et les facteurs AP-1." Montpellier 1, 2000. http://www.theses.fr/2000MON1T007.