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Статті в журналах з теми "Altérations de facteurs de transcription"
Bensellam, M., Y. Guiot, D. R. Laybutt, and J. C. Jonas. "O50 Rôle de l’hypoxie et des facteurs de transcription HIF1 et HIF2 dans les altérations glucotoxiques de l’expression génique dans les cellules pancréatiques." Diabetes & Metabolism 36 (March 2010): A13—A14. http://dx.doi.org/10.1016/s1262-3636(10)70054-9.
Повний текст джерелаLa Spada, F., V. Mongrain, T. Curie, and P. Franken. "La perte de sommeil entraîne une altération de la liaison des facteurs de transcriptions circadiens à l’ADN." Médecine du Sommeil 9, no. 2 (April 2012): 44–45. http://dx.doi.org/10.1016/j.msom.2012.04.014.
Повний текст джерелаLa Spada, F., V. Mongrain, T. Curie, and P. Franken. "La perte de sommeil entraîne une altération de la liaison des facteurs de transcriptions circadiens à l’ADN." Neurophysiologie Clinique/Clinical Neurophysiology 42, no. 3 (April 2012): 143–44. http://dx.doi.org/10.1016/j.neucli.2012.02.014.
Повний текст джерелаLorenzo, Hans-Kristian, and Jean-Jacques Candelier. "Syndrome néphrotique idiopathique et facteurs circulants." médecine/sciences 35, no. 8-9 (August 2019): 659–66. http://dx.doi.org/10.1051/medsci/2019128.
Повний текст джерелаScoazec, Jean-Yves. "Facteurs de transcription : quelles applications diagnostiques ?" Annales de Pathologie 32, no. 5 (November 2012): S32—S33. http://dx.doi.org/10.1016/j.annpat.2012.08.003.
Повний текст джерелаCottencin, O. "Des altérations neuropsychologiques à la remédiation dans les addictions." European Psychiatry 29, S3 (November 2014): 533. http://dx.doi.org/10.1016/j.eurpsy.2014.09.394.
Повний текст джерелаKahn, A. "Domaine POU-homéo et facteurs de transcription." médecine/sciences 5, no. 3 (1989): 172. http://dx.doi.org/10.4267/10608/3940.
Повний текст джерелаBlumenfeld, M., and M. Vasseur. "Oligonucléotides "sens" : ligands rationnels des facteurs de transcription." médecine/sciences 10, no. 3 (1994): 274. http://dx.doi.org/10.4267/10608/2605.
Повний текст джерелаKahn, A. "Leucémies et oncogènes : des facteurs de transcription hybrides." médecine/sciences 6, no. 5 (1990): 489. http://dx.doi.org/10.4267/10608/4177.
Повний текст джерелаMaizel, Alexis. "Mouvement de facteurs de transcription chez les plantes." Journal de la Société de Biologie 200, no. 3 (2006): 221–27. http://dx.doi.org/10.1051/jbio:2006025.
Повний текст джерелаДисертації з теми "Altérations de facteurs de transcription"
Duployez, Nicolas. "Etude des altérations génomiques acquises dans les leucémies aiguës myéloïdes impliquant le core binding factor." Thesis, Lille 2, 2017. http://www.theses.fr/2017LIL2S037/document.
Повний текст джерелаRUNX1 and CBFB encode subunits of the core binding factor (CBF), a heterodimeric transcription factor required for the establishment of definitive hematopoiesis. Deregulation of the CBF is one of the most frequent aberrations in hematological malignancies. Since CBF disruption alone is insufficient to induce acute myeloid leukemia (AML) on its own, AML with CBF involvement is considered as a model of multistep leukemogenesis requiring additional genetic aberrations.Here, we focused on acute myeloid leukemia (AML) with t(8;21)/RUNX1-RUNX1T1 fusion and AML with inv(16)/CBFB-MYH11 fusion, reported together as CBF AML, as well as AML with germline RUNX1 mutation (defining the familial platelet disorder with propensity to develop leukemia or FPD/AML).In order to explore additional genomic aberrations, we performed comprehensive genetic profiling in CBF AML patients enrolled in the French trials ELAM02 (0-18 years) and CBF2006 (18-60 years) using both high-throughput sequencing (n=215) and single nucleotide polymorphism-array (n=198). In addition, we sequenced samples from 25 individuals with FPD/AML (15 pedigrees) diagnosed between 2005 and 2014 at thrombocyto-penic stage and during leukemic progression.In CBF AML, mutations in genes activating tyrosine kinase (TK) signaling were frequent in both subtypes as previously described by others. By contrast, we found mutations in genes encoding chromatin modifiers or members of the cohesin complex with high frequencies in t(8;21) AML (41% and 18% respectively) while they were nearly absent in inv(16) AML. Interestingly, such mutations were associated with a poor prognosis in patients with TK mutations suggesting synergic cooperation between these events. Other events included ZBTB7A and DHX15 mutations in t(8;21) AML (20% and 6% respectively) and FOXP1 deletions or truncating mutations in inv(16) AML (7%). Finally, we described CCDC26 disruption as a possible new lesion associated with aberrant TK signaling in this particular subtype of leukemia (4.5% of CBF AML).In FPD/AML, mutational analysis revealed the acquisition of a second event involving RUNX1 in all patients with AML including somatic mutation of the second allele or duplication of the germline RUNX1 mutation through copy-neutral loss of heterozygosity and trisomy 21. In clinical practice, we suggest that the occurrence of two different RUNX1 mutations or a single RUNX1 mutation with a variant allele frequency higher than 50% in a patient with AML should alert about the possibility of FPD/AML
Brunet, Julie. "Altérations épigénétiques et rôle du facteur de transcription UHRF1 dans les cellules-hôtes infectées par Toxoplasma gondii." Strasbourg, 2010. https://publication-theses.unistra.fr/public/theses_doctorat/2010/BRUNET_Julie_2010.pdf.
Повний текст джерелаToxoplasmosis, caused by a parasite, Toxoplasma gondii, is one of the most common infections in France:about 50% of the adult population is infected and it is estimated that 200,000-300,000 new infections occur each year, 15-20% which are symptomatic. The severity of infection is due to the risk of fetal transmission of the parasite in cases of infection during pregnancy and the risk of reactivation in the case of immunosuppression. There is no efficient treatment for the intracellular forms of the parasite and no vaccine. T. Gondii is an obligate intracellular parasite that interferes with the molecular signaling pathways of host cells and alters several physiological processes such as differentiation, apoptosis and proliferation. The transcription factor UHRF1 (ubiquitin-like, containing PHD and RING finger domains, 1) is a key cell cycle regulator. It’s also a "methyl-CpG-binding protein” that gives it a crucial role in the replication of the epigenetic code. The molecular mechanisms by which the parasite affects the host cell remain poorly understood. We observed that infection with T. Gondii leads to an inhibition of proliferation of host cells due to cell cycle arrest in G2 phase. This results in a decrease of expression of cyclin B and a sharp increase in UHRF1 in host cells. Inhibition of UHRF1 by SiRNA in host cells induces a significant decrease in parasite growth. We observed an increase in binding of UHRF1 to cyclin B promoter during infection with T. Gondii. UHRF1 could be responsible for the repression of cyclin B gene, leading to cell cycle arrest. T. Gondii is able to modulate gene expression by interfering with two important epigenetic modifications, methylation and histone modifications. UHRF1 is a transcription factor that connects these two epigenetic modifications. This would make UHRF1 a powerful tool that would allow the parasite to exploit the genome of the host cell. Activating UHRF1 involved the transcription factor NF-kB and a factor based on the parasite rhoptries
Ruiz, Emmanuelle. "Coopération entre les inducteurs de l’EMT (EMT-TF/miRNA) et les altérations oncogéniques dans la tumorigenèse mammaire." Thesis, Lyon 1, 2015. http://www.theses.fr/2015LYO10069.
Повний текст джерелаCancer cells are able to reactivate the Epithelio-Mesenchymal Transition (EMT), an embryonic mechanism, to acquire mobility and dedifferentiation capacities. EMT leads to a genetic reprogramming with the reactivation of EMT inductors, mainly transcription factors (EMT-TF) and the inhibition of miRNA. Otherwise, oncogenic stresses are essentials to tumor progression. The aim of my thesis project was to have a better understanding about the cooperation between events of genetic reprogramming occurring during EMT and oncogenic stresses during mammary tumor transformation. First, a screening based on oncogenic cooperation in soft agar assay, between EMT-TFs and oncogenic stresses was performed. Following a bioinformatics analysis, different EMT-TFs signatures associated with an oncogenic stress were identified. Thus, for example, the expression of EMT-TF ZEB1 and GSC were associated with the deletion of tumor suppressor gene PTEN to transform immortalized mammary epithelial cells. An immunohistochemistry analysis on a set of 558 triple negative breast cancers validated in vivo the presence of a correlation between the expressions of GSC and PTEN. However, this association seems to be more complex. Indeed, the expression of GSC is negatively associated with the nuclear expression of PTEN while it’s positively associated with the cytoplasmic expression of PTEN. Finally, an analysis of public metadata on cancer samples as TCGA or METABRIC is ongoing to validate these in vitro signatures and wider to determine how EMT or EMT-TFs associated signatures correlate with classical oncogenic pathways.Secondly, an in silico analysis, from predictive algorithms of miRNA targets, was performed to select miRNA able to inhibit the expression of several EMT-TFs. Two miRNA (miR-495 and miR-590-3p) were identified targeting several members of four principal’s families of EMT-TFs (FOXC, Snail, bHLH and ZEB). In vitro tests were realized to validate these regulations identifying Slug as a target of miR-590-3p. Moreover, these miRNAs expression in mammary cell lines is negatively correlated with EMT-TFs expression and EMT markers. A treatment with TGF-, a major EMT inductor, decreases their expression, potentially meaning that these miRNA can negatively regulate EMT. In parallel, several EMT-TFs are able to repress the expression of miR-590-3p, acting directly on its promotor, thus creating feedback loops. Functional studies using stable expression vector of miR-590-3p suggest a secondary role of this miRNA in the regulation of EMT because miR-590-3p deregulates EMT secondary markers as N-Cadherin. Functions restauration studies are planned to determine how important these feedback loops in mammary tumor progression are. To open the project, expression of these identified miRNA will be correlated with EMT-TF associated signatures and with classical oncogenic pathways to determine the link between these three components in mammary tumorigenesis. My thesis works are shown that there is an interactome between EMT inductors, oncogenic stresses and miRNA during human mammary transformation
Jamrog, Laura. "Impact des altérations génétiques de PAX5 sur le développement de la lignée lymphoïde B et dans la leucémogenèse des LAL-B." Electronic Thesis or Diss., Toulouse 3, 2021. http://www.theses.fr/2021TOU30306.
Повний текст джерелаThe PAX5 (Paired boX 5) gene encodes a key transcription factor crucial for B-cell differentiation. We showed that the two PAX5 isoforms are differentially regulated but have equivalent function during early B-cell differentiation. Indeed, PAX5A and PAX5B isoforms can both induce B-cell program but may have functional differences after B-cell activation. The tight control of their expression may thus reflect a way to finely tune PAX5 dosage during B-cell differentiation process. PAX5 is a well-known haploinsufficient tumor suppressor gene in human B-cell precursor acute lymphoblastic leukemia (BCP-ALL) and is the main target of a wide diversity of somatic alterations in childhood and adult BCP-ALL, occurring in one third of sporadic cases. However, the role of PAX5 fusion proteins in BCP-ALL initiation and transformation is ill-known. We previously reported a new recurrent t(7;9)(q11;p13) chromosomal translocation in human BCP-ALL that juxtaposed PAX5 to the coding sequence of elastin (ELN). To study the function of the resulting PAX5-ELN fusion protein in BCP-ALL development, we generated a mouse model in which the PAX5-ELN transgene is expressed specifically in B cells. PAX5-ELN-expressing mice efficiently developed BCP-ALL phenotype with a penetrance of 80%. Leukemic transformation was associated with clonal Immunoglobulin gene rearrangement and recurrent secondary mutations in Ptpn11, Kras, Pax5, and Jak3 genes affecting key signaling pathways required for cell proliferation. Our functional studies demonstrated that PAX5-ELN impairs B-cell development in vitro and in vivo and induces an aberrant expansion of the pro-B cell compartment at the preleukemic stage. Our molecular and computational approaches identified PAX5-ELN-regulated candidate genes that establish the molecular bases of the preleukemic state to drive BCP-ALL initiation. In conclusion, our study provides a new in vivo model recapitulating the multistep leukemogenesis process of human BCP-ALL and strongly implicates PAX5 fusion proteins as potent oncoproteins in leukemia development. Furthermore, there is increasing evidence for an inherited genetic basis of susceptibility to childhood BCP-ALL. In this context, four unrelated families with childhood BCP-ALL expressing heterozygous PAX5 germline point mutations were recently reported: the recurrent mutation PAX5 G183S affecting the octapeptide domain of PAX5 has been described in three families while PAX5 R38H affecting its DNA-binding paired domain has been identified in another one. We strengthen the hypothesis of inherited character of familial BCP-ALL with the description of three novel familial BCP-ALL cases in related patients that express the germline PAX5 R38H mutation. To uncover the intrinsic effect of PAX5 R38H mutant in B-cell development, we performed in vitro, and in vivo functional assays combined with a gene expression analysis, based on a retroviral complementation approach. Our results indicated that PAX5 R38H mutant acts as a strong hypomorphic variant that fails to drive B-cell differentiation and does not exert a dominant-negative effect on wild-type PAX5. Syngeneic transplantation of PAX5 R38H-expressing cells demonstrated maintenance of engraftment capacity and led to development of BCP-ALL phenotype in mice. Our transcriptomic analysis of these PAX5 R38H-expressing cells showed that PAX5 R38H drastically alters the pattern of expression of PAX5 target genes but also revealed a distinct molecular signature specific to PAX5 R38H. Together with previous unrelated family study, our observations allow to establish the recurrence of the germline PAX5 R38H mutation associated with BCP-ALL. Our data also highlight the importance of transcriptional dysregulation in leukemogenesis of familial BCP-ALL, particularly of genes involved in B-cell differentiation
Sérandour, Aurélien. "Dynamique de méthylation et d’hydroxyméthylation de l’ADN des enhancers au cours de la différenciation cellulaire in vitro." Rennes 1, 2011. http://www.theses.fr/2011REN1S074.
Повний текст джерелаTranscriptome and cis-tridimensional positioning of chromatin domains undergo deep modifications during cell differentiation and reprogramming. In embryonic stem cells, master genes such as Pou5f1/Oct4, Nanog, Sox2 and Klf4 are implicated in a regulatory network which builds a pluripotent chromatin. This chromatin can be modified in a cell fate-specific manner during differentiation, allowing specialization and restriction of gene expression patterns. Specific enhancers bound by de novo expressed transcription factors become activated during this process. Using epigenomic mapping technologies in different cell lines, we observed that DNA of active enhancers is hypomethylated and that DNA of activated enhancers can be de novo hydroxymethylated during in vitro cell differentiation
Dubaele, Sandy. "Importance de la sous-unité XPD pour l'architecture et les activités du facteur de transcription-réparation TFIIH." Université Louis Pasteur (Strasbourg) (1971-2008), 2003. http://www.theses.fr/2003STR13136.
Повний текст джерелаFan, Jun. "Single-molecule basis of transcription-coupled DNA repair." Sorbonne Paris Cité, 2015. http://www.theses.fr/2015USPCC213.
Повний текст джерелаThe DNA in living cells is constantly threatened by damages from both endogenous and exogenous agents, which can threaten genomic integrity, block processes of replication, transcription and translation and have also genotoxic effects. In response to the DNA damage challenge, organisms have evolved diverse surveillance mechanisms to coordinate DNA repair and cell-cycle progression. Multiple DNA repair mechanisms, discovered in both prokaryotic and eukaryotic organisms, bear the responsibility of maintaining genomic integrity; these mechanisms include nucleotide excision repair (NER), base excision repair (BER), mismatch repair (MMR) and double strand break repair (DSBR). Transcription-coupled DNA repair (TCR) is a specialized NER subpathway characterized by enhanced repair of the template strand of actively transcribed genes as compared to the classical global genome repair (GGR) subpathway of NER which does not distinguish between template and non-template strands. TCR achieves specialization via the involvement of RNA polymerase (RNAP) and the Mfd (Mutation Frequency Decline) protein, also known as TRCF (transcription repair coupling factor). TCR repair initiates when RNAP stalls at a DNA lesion on the transcribed strand and serves as the da mage sensor. The stalled RNAP must be displaced so as to make the lesion accessible to downstream repair components. E. Coli Mfd translocase participates in this process by displacing stalled RNAP from the lesion and then coordinating assembly of the UvrAB(C) components at th( damage site. Recent studies have shown that after binding to and displacing stalled RNAP, Mfd remains on the DNA in the form of a stable, translocating complex with evicted RNAP. So as to understand how UvrAB(C) are recruited via the Mfd-RNAP complex, magnetic trapping of individual, damaged DNA molecules was employed to observe-in real-time this multi¬component, multi-step reaction, up to and including the DNA incision reaction by UvrC. It was found that the recruitment of UvrA and UvrAB to the Mfd-RNAP complex halts the translocating complex and then causes dissolution of the complex in a molecular "hand-off" with slow kinetics Correlative single-molecule nanomanipulation and fluorescence further show that dissolution of the complex leads to loss of not only RNAP but also Mfd. Hand-off then allows for enhanced incision of damaged DNA by the UvrC component as compared to the equivalent single-moleculE GGR incision reaction. A global model integrating TCR and GGR components in repair was proposed, with the overall timescales for the parallel reactions provided
Benko, Sabina. "Altérations génomiques à grande distance d'éléments non-codants conservés et dérégulation d'expression tissu-spécifique au locus SOX9." Paris 5, 2010. http://www.theses.fr/2010PA05T039.
Повний текст джерелаSQX9 is a major developmental gene mapping to a vast gene desert that encompasses its regulatory domain. The SOX9 gene coding equence mutations result in campomelic dysplaisa (CD), a complex polymalformative syndrome. We showed that alterations of non-coding sequences (translocations, deletions or point mutations) at the SOX9 locus result in isolated CD endophenotypes namely Pierre Robin sequence (iPRS) and disorders of sex developpement (iDSD). Both in vitro and in vivo studies indicate that those alterations, located at great distance with respect to SOX9 coding sequences (>1,2Mb/iPRS; >500kb/iDSD), comprise regions conserved throughout the evolution that function as regulatory elements driving tissue specific gene expression of SOX9. We suggest that alterations identified in iPRS and iDSD patients represent a tissue specific loss of SOX9 expression in the mandibular mesenchyme or the developing gonad respectively, while other territories of normal SOX9 expression remain intact
Zerdoumi, Yasmine. "Analyse fonctionnelle des mutations constitutionnelles hétérozygotes du gène suppresseur de tumeur TP53 dans le contexte génétique des patients atteints du syndrome de Li-Fraumeni." Rouen, 2016. http://www.theses.fr/2016ROUES035.
Повний текст джерелаLi-Fraumeni Syndrome (LFS), resulting from heterozygous germline mutations of TP53, is one of the most severe hereditary cancer syndromes. In order to determine the molecular basis of the clinical gradient of germline TP53 mutations, we studied the functional consequences of the different types of TP53 mutations in the genetic context of the patients, and we showed that TP53 missense mutations with dominant-negative effect alter the p53 transcriptional response to DNA damage more drastically than null mutations. These results indicate that the impact of the mutations on p53 transcriptional response to DNA damage in LFS lymphocytes can be considered as an endophenotype of the clinical severity of germline TP53 mutations. The use of the simple p53 functional assay allowed us to confirm these observations on a large number of mutations. ChIP-Seq analysis performed on lymphocytes derived from TP53 wild-type control subject and LFS patient with TP53 dominant-negative missense, showed that the drastic alteration of p53 transcriptional response to DNA in LFS lymphocytes harboring dominant negative missense mutations, is explained by a massive and global alteration of p53 DNA binding. In order to determine the causative role of chemotherapies in the appearance of secondary tumours in LFS, we developed a new genotoxicity assay, named the p53 genotoxicity assay. This assay allowed us to show that most of the drugs commonly used in cancer treatment, except the microtubule poisons, are highly genotoxic. Thus, in TP53 mutation carriers, germline TP53 mutations represent a genetic permissive context facilitating the malignant transformation of cells in which DNA damage has occurred
Gosselin, Karo. "Étude de l'implication du stress oxydant induit par les facteurs Rel/NF-kappaB dans la sénescence et l'émergence tumorale." Lille 1, 2005. https://pepite-depot.univ-lille.fr/RESTREINT/Th_Num/2005/50376-2005-75.pdf.
Повний текст джерелаКниги з теми "Altérations de facteurs de transcription"
1947-, Locker Joseph, ed. Transcription factors. Oxford: BIOS, 2001.
Знайти повний текст джерелаStephen, Goodbourn, ed. Eukaryotic gene transcription. Oxford: IRL Press at Oxford University Press, 1996.
Знайти повний текст джерелаLatchman, David S. Eukaryotic transcription factors. 5th ed. Amsterdam: Elsevier/Academic Press, 2008.
Знайти повний текст джерелаEukaryotic transcription factors. 4th ed. Oxford: Academic, 2004.
Знайти повний текст джерелаLatchman, David S. Eukaryotic transcription factors. 5th ed. Great Britain: Academic Press, 2008.
Знайти повний текст джерелаE, Angel Peter, and Herrlich Peter 1940-, eds. The fos and jun families of transcription factors. Boca Raton: CRC Press, 1994.
Знайти повний текст джерелаT, Smale Stephen, and NetLibrary Inc, eds. Transcriptional regulation in eukaryotes: Concepts, strategies, and techniques. Cold Spring Harbor, NY: Cold Spring Harbor Laboratory Press, 2000.
Знайти повний текст джерелаB, La Thangue Nicholas, and Bandara Lasantha R, eds. Targets for cancer chemotherapy: Transcription factors and other nuclear proteins. Totowa, N.J: Humana Press, 2002.
Знайти повний текст джерелаB, La Thangue Nicholas, and Bandara Lasantha R, eds. Targets for cancer chemotherapy: Transcription factors and other nuclear proteins. Totowa, N.J: Humana Press, 2002.
Знайти повний текст джерелаNATO Advanced Study Institute on Molecular Mechanisms of Signal Transduction (1999 Spetsai Island, Greece). Molecular mechanisms of signal transduction. Amsterdam: IOS Press, 2000.
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