Relevant bibliographies by topics / Facteur de transcription NF-kB

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Academic literature on the topic 'Facteur de transcription NF-kB'

Author: Grafiati
Published: 4 June 2021
Last updated: 7 February 2022

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Journal articles on the topic "Facteur de transcription NF-kB"

1

Stephenson, Diane, Tinggui Yin, E. Barry Smalstig, Mei Ann Hsu, Jill Panetta, Sheila Little, and James Clemens. "Transcription Factor Nuclear Factor-Kappa B is Activated in Neurons after Focal Cerebral Ischemia." Journal of Cerebral Blood Flow & Metabolism 20, no. 3 (March 2000): 592–603. http://dx.doi.org/10.1097/00004647-200003000-00017.

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Nuclear factor-kappa B (NF-kB) is a multisubunit transcription factor that when activated induces the expression of genes encoding acute-phase proteins, cell adhesion molecules, cell surface receptors, and cytokines. NF-kB is composed of a variety of protein subunits of which p50-and p65-kDa (RelA) are the most widely studied. Under resting conditions, these subunits reside in the cytoplasm as an inactive complex bound by inhibitor proteins, IkBα and IkBβ. On activation, IkB is phosphorylated by IkB kinase and ubiquitinated and degraded by the proteasome; simultaneously, the active heterodimer translocates to the nucleus where it can initiate gene transcription. In the periphery, NF-kB is involved in inflammation through stimulation of the production of inflammatory mediators. The role of NF-kB in the brain is unclear. In vitro, NF-kB activation can be either protective or deleterious. The role of NF-kB in ischemic neuronal cell death in vivo was investigated. Adult male rats were subjected to 2 hours of focal ischemia induced by middle cerebral artery occlusion (MCAO). At 2, 6, and 12 hours after reperfusion, the expression and transactivation of NF-kB in ischemic versus nonischemic cortex and striatum were determined by immunocytochemistry and by electrophoretic mobility gel-shift analysis. At all time points studied, p50 and p65 immunoreactivity was found exclusively in the nuclei of cortical and striatal neurons in the ischemic hemisphere. The contralateral nonischemic hemisphere showed no evidence of nuclear NF-kB immunoreactivity. Double immunofluorescence confirmed expression of p50 in nuclei of neurons. Increased NF-kB DNA-binding activity in nuclear extracts prepared from the ischemic hemisphere was further substantiated by electrophoretic mobility gel-shift analysis. Because the activation of NF-kB by many stimuli can be blocked by antioxidants in vitro, the effect of the antioxidant, LY341122, previously shown to be neuroprotective, on NF-kB activation in the MCAO model was evaluated. No significant activation of NF-kB was found by electrophoretic mobility gel-shift analysis in animals treated with LY341122. These results demonstrate that transient focal cerebral ischemia results in activation of NF-kB in neurons and supports previous observations that neuroprotective antioxidants may inhibit neuronal death by preventing the activation of NF-kB.
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Komakh, Y. A., S. A. Borzenok, T. V. Radygina, D. G. Kuptsova, and S. V. Petrichuk. "Transcription factor NF-kB in the prognosis of outcomes for patients undergoing repeat keratoplasty." Oftalmologicheskii Zhurnal 91, no. 2 (April 16, 2021): 16–22. http://dx.doi.org/10.31288/oftalmolzh202121622.

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Hewamana, Saman, Mathew Clement, Thet Thet Lin, Chris Jenkins, Chris Fegan, Clare Rowntree, Paul Brennan, and Chris Pepper. "Transcription Factor NF-kB as a Biomarker for Disease Progression and Target for Treatment in Chronic Lymphocytic Leukaemia." Blood 110, no. 11 (November 16, 2007): 3091. http://dx.doi.org/10.1182/blood.v110.11.3091.3091.

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Abstract NF-kB is part of a multi-component signalling pathway that regulates the expression of hundreds of genes involved in the control of cell proliferation, cell survival, stress responses, innate immunity and inflammation. The principal constituents of mammalian NF-kB are p65, p50, p52, c-Rel and Rel-B and in their inactive state they are bound in the cytoplasm to the inhibitor protein IKB. Phosphorylation of IKB by IKB kinase has been shown to result in the translocation of NF-kB into the nucleus where it can bind to kB responsive elements. It has been reported that NF-kB is constitutively activated in chronic lymphocytic leukaemia (CLL) cells. However, no previous studies have prospectively quantified the subunits of NF-kB in primary CLL cells or examined their relative expression between patient samples. Therefore, the aim of our study was to perform quantitative subunit analysis of NF-κB in freshly isolated CLL cells and examine their relationship with some of the well established clinical and molecular prognostic markers. NF-κB was evaluated using EMSA (n= 48), supershift assays and p65 subunit-specific ELISA (n=100). Apoptosis was measured at 24h and 48h using annexin V/propidium iodide labelling. We demonstrated a wide variation in NF-κB expression in CLL samples and p50, p65 and c-rel were consistently shown to be the predominant NF-kB subunits. Importantly, we showed a negative correlation between in vitro apoptosis and nuclear p65 NF-kB expression (r2 = −0.22) suggesting that high levels of p65 confer a cytoprotective effect on primary CLL cells. Furthermore, we found that p65 has a positive correlation (r2 = 0.3) with total white cell count (WBC) and CLL samples with a lymphocyte doubling time below 12 months have significantly higher p65 DNA binding (p= 0.02) implicating this NF-κB subunit in disease progression. Finally we have also demonstrated that the NF-κB inhibitor, LC-1, has potent in vitro apoptosis-inducing effects on primary CLL cells. Together, this work supports the use of specific inhibitors of NF-kB, particularly targeting p65, for treatment of CLL.
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Colombo, Jucimara, Bruna V. Jardim-Perassi, João P. S. Ferreira, Cristine Z. Braga, Nathália M. Sonehara, Rubens P. Júnior, Marina G. Moschetta, Ana P. Girol, and Debora A. P. C. Zuccari. "Melatonin Differentially Modulates NF-кB Expression in Breast and Liver Cancer Cells." Anti-Cancer Agents in Medicinal Chemistry 18, no. 12 (January 29, 2019): 1688–94. http://dx.doi.org/10.2174/1871520618666180131112304.

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Background: NF-kB (nuclear factor kappa B) is a transcription factor composed of two subunits, p50 and p65, which plays a key role in the inflammatory process. Melatonin has oncostatic, antiangiogenic and antimetastatic properties, and some recent studies have indicated an inhibitory effect of melatonin on NF-kB in some types of cancer. This work aims to investigate the effects of melatonin treatment on the expression of NFkB in breast and liver cancer models. Method: The breast cancer xenographic model was performed using female Balb/c nude athymic mice injected with MDA-MB-231 cells. The animals were treated with 40 mg/Kg of melatonin for 21 days. Volume of the tumors was measured with a digital caliper. Hepatocarcinoma model was developed by using the HepG2 cells in vitro, treated with 1 mM melatonin for 24 h. The expression of NF-kB protein was verified by immunohistochemistry and immunocytochemistry and quantified by optical densitometry, in vivo study and in vitro study, respectively. NF-kB gene expression was performed by quantitative RT-PCR. Results: The breast cancer xenografts nude mice treated with melatonin showed reduced tumor size (P=0.0022). There was a decrease in NF-kB protein staining (P=0.0027) and gene expression (P=0.0185) in mice treated with melatonin. The opposite results were observed for the hepatocarcinoma model. HepG2 cells treated with melatonin showed an increase in the NF-kB immunostaining when compared to control cells (P=0.0042). Conclusion: Our results indicated that the treatment with melatonin was able to decrease both gene and protein expressions of NF-kB in breast cancer cells and, conversely, increase the transcription factor protein expression in hepatocarcinoma cells. These data highlighted a double role in the expression of NF-kB, depending on the cell type. Further studies are needed to better elucidate the action of melatonin in NF-kB, since this transcription factor acts on different signaling pathways that are fundamental for carcinogenesis.
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Geng, Jian-Guo, Jian-Guo Wang, Nigel Mackman, Arne Slungaard, Yuqing Huo, and Nigel S. Key. "Regulation of Tissue Factor by NF-kB Transcription Factor p50 Is Essential for the Pathogeneses of Deep Vein Thrombosis and Arterial Restenosis." Blood 108, no. 11 (November 16, 2006): 1458. http://dx.doi.org/10.1182/blood.v108.11.1458.1458.

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Abstract NF-kB transcription factors regulate the expression of tissue factor (TF), a principal initiator for the coagulation cascade. Dominant among the five cellular members of NF-kB transcription factors is the p50/p65 heterodimer. Here we report that Andrographolide (Andro; a 350-dalton antagonist that targets reduced cysteine62 of p50 for inhibition of NF-kB activation) and genetic deletion of p50 potently attenuated TF activity in stimulated endothelial cells and monocytes/macrophages. The direct binding of p50/p65 heterodimer to the TF-kB site in human TF promoter was demonstrated by p50 and p65 antibody ‘supershift’ using electrophoretic mobility shift assay and immunoprecipitation of the promoter of the human TF gene from chromatins of TNF-a-stimulated human umbilical vein endothelial cells. Andro-treated and p50 null mice both exhibited suppressed TF expression, blunted fibrin deposition, reduced venous thrombosis, and decreased neointimal hyperplasia. Blockade of TF activity by an anti-murine TF antibody also attenuated venous thrombosis and neointimal proliferation in vivo. Our findings thus indicate that NF-kB transcription factor p50 critically regulates TF activity in the pathogeneses of deep vein thrombosis and arterial restenosis, and suggest that specific inhibitors of p50, such as Andro, have the potential to be therapeutically valuable for preventing and perhaps treating arterial and venous thrombosis.
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CILIBERTO, G., A. DEMARTIS, and B. MAJELLO. "IL-1 induces transcription factor NF-kB in hepatoma cells." Cell Biology International Reports 14 (September 1990): 55. http://dx.doi.org/10.1016/0309-1651(90)90325-s.

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7

Tiedemann, Rodger E., Jonathan J. Keats, Jessica Schmidt, Chang-Xin Shi, Yuan X. Zhu, Xinliang Mao, Aaron D. Schimmer, and Keith Stewart. "Identification of a Potent Natural Triterpenoid Inhibitor of Proteosome Chymotrypsin-Like Activity and NF-κB with Specific Anti-Myeloma Activity in Vitro and in Vivo." Blood 112, no. 11 (November 16, 2008): 3679. http://dx.doi.org/10.1182/blood.v112.11.3679.3679.

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Abstract As multiple myeloma tumors universally dysregulate cyclin D genes we conducted high-throughput chemical library screens for compounds that inhibit signaling pathways driving cyclin D2 promoter transactivation, assaying more than 4,000 compounds. The top-ranked compound from these studies was a natural triterpenoid, pristimerin. Pristimerin markedly suppressed cyclin D2 promoter activity (>90%) in 3T3 fibroblast cells and inhibited cyclin D1, D2 and D3 protein expression in myeloma tumor cells. Strikingly, the early (4 hour) transcriptional response of myeloma cells treated with pristimerin closely resembles cellular responses elicited by proteosome inhibitors (P<10−9) (Connectivity Map Build 2, www.broad.mit.edu/cmap), with rapid induction of heat shock proteins (HSP70 >90-fold), activating transcription factor (ATF) 3 and CHOP. Enzymatic assays performed with purified 20S proteosome, or with total cellular extract, confirm that pristimerin rapidly and specifically inhibits chymotrypsin-like 20S proteosome activity at low concentration (<100nM), causing sustained inhibition lasting >6 hours. Consistent with inhibition of proteosome function, pristimerin causes rapid and sustained accumulation of high molecular weight poly-ubiquitinated protein in myeloma cell lines. Notably, related cytotoxic triterpenoid drugs, such as the methyl ester of 2-cyano-3,12-dioxooleana-1,9(11)-dien-28-oic acid (CDDO-Me, RTA 402) or betulinic acid or the ginsenosides - all of which show promising anti-cancer activities and are currently in clinical trials for advanced lymphoma, leukemia or solid malignancies - commonly inhibit NF-kB activation via direct inhibition of IKKα or IKKβ. In contrast drugs that function as proteosome inhibitors also commonly suppress NF-kB function instead by impairing degradation of ubiquitinated IkB. Immunoblotting for phosphorylated IkB confirms that pristimerin, like other triterpenoids, acts upstream of IkB to inhibit its phosphorylation, although pristimerin simultaneously inhibits proteosome activity with marked potency to diminish the clearance of ubiquitinated IkB. As a result of this two-fold stabilization of IkB, pristimerin causes overt and specific suppression of NF-kB mediated transcription, measured by a panel of transcriptional reporters with synthetic promoters containing 5x repeats of generic binding sites for NF-kB, AP-1, CREB or TCF4. Importantly, specific suppression of constitutive NF-kB transcriptional activity was pronounced in myeloma cells with inherent NF-kB pathway activation resulting from bi-allelic deletion of the TRAF3 tumor suppressor. Constitutive activation of the NF-kB pathway occurs in a significant proportion of primary myeloma tumors, most commonly via inactivation of TRAF3. Selective silencing of NF-kB driven transcription in myeloma cells may mediate the potent suppression of cyclin D proteins induced by this compound. Significantly, multiple myeloma cells are exquisitely sensitive to both proteosome inhibition or NFkB pathway inhibition. Consistent with these twin vulnerabilities, pristimerin is potently and selectively lethal to primary myeloma cells from patients (IC50<100nM) grown in mixed lineage culture and inhibits the growth of xenografted human plasmacytoma tumors grown in mice, providing a strong rationale for pharmaceutical development of triterpenoid dual-function proteosome-plus-NF-kB pathway inhibitors as therapeutics for multiple myeloma and related human malignancies.
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Wagner, Amy J., Erin K. Hertlein, Chelsey A. Raymond, Derek A. West, Joseph M. Flynn, Thomas Lin, Amy J. Johnson, and John C. Byrd. "17-DMAG Targets the NF-κB Family of Proteins to Induce Apoptosis in CLL: Clinical Implications of Hsp90 Inhibition." Blood 112, no. 11 (November 16, 2008): 381. http://dx.doi.org/10.1182/blood.v112.11.381.381.

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Abstract Chronic lymphocytic leukemia (CLL) is a disease of accumulating B-cell lymphocytes for which there is currently no curative therapy. One attractive therapeutic target currently being explored in CLL is Hsp90, a chaperone which stabilizes various client proteins (Akt, Raf, ZAP-70) which are important for survival of CLL cells. Interfering with Hsp90 protein binding to these chaperone proteins leads to their rapid degradation. Our group and others have demonstrated that 17-allylamino-17-demethoxy-geldanamycin (17-AAG) depletes only select chaperone proteins and promotes only modest cytotoxicity in CLL. 17-dimethylaminoethylamino-17-demethoxy-geldanamycin (17-DMAG) is a novel Hsp90 inhibitor with improved solubility, bioavailability and cytotoxicity in other cancer cell lines as compared to 17-AAG. We demonstrate that 17-DMAG more potently induces caspase dependent apoptosis of primary CLL cells, as compared to 17-AAG, but does not mediate apoptosis of normal T-cells and NK-cells. In primary CLL cells, 17-DMAG treatment leads to cellular depletion of a broader range of Hsp90 client proteins (Akt, Cdk9, ZAP-70 and IKK). IKK is the activating kinase of the NF-kB family of transcription factors. To validate the down-stream significance of this we used EMSA to confirm that NF-kB is constitutively active in CLL as compared to normal B-cells. We demonstrate that 17-DMAG effectively reduces NF-kB DNA binding and thereby decreases subsequent transcription of known NF-kB target genes (Mcl-1 and XIAP). In addition to the direct role of NF-kB on target genes, NF-kB inhibition indirectly increases Bim transcription through regulation of the FoxO3a transcription factor. Furthermore, the reciprocal regulation transcription of Bcl-2 family members Mcl-1 and Bim are early events that initiate membrane depolarization and activation of the caspase cascade, leading to 17-DMAG induced cytotoxicity. siRNA experiments to elucidate the direct importance of Bim to 17-DMAG treatment are ongoing at this time. In conclusion, our data demonstrate that the Hsp90 inhibitor 17-DMAG represents a novel multi-targeted inhibitor of several critical kinases, transcription factors and anti-apoptosis genes relevant to CLL survival. Given its oral formulation, which allows administration of 17-DMAG by continuous dosing and uninterrupted inhibition of Hsp90, initiation of phase II clinical trials in CLL that include detailed pharmacodynamic studies monitoring NF-kB target genes are indicated. This work is supported by the Leukemia and Lymphoma Society of America and the D. Warren Brown Foundation.
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Agarwal, Nitin Kumar, Chae Hwa Kim, Kranthi Kunkalla, Izidore S. Lossos, and Francisco Vega. "The Inhibitor of NF-KB Kinase, IKKβ Regulates the Transcriptional Activity of GLI1 By Blocking Its Proteasomal Degradation." Blood 124, no. 21 (December 6, 2014): 2199. http://dx.doi.org/10.1182/blood.v124.21.2199.2199.

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Abstract GLI1 is a Hedgehog (Hh) related transcription factor originally discovered as an amplified product in gliomas. Inappropriate activation of the GLI1 has been shown in many cancers including diffuse large B cell lymphoma (DLBCL). We previously showed that GLI1 mediated canonical Hh signaling is constitutive active in DLBCL and contributes to cell survival, proliferation and enhances chemotolerance. Although the importance of GLI1 in tumor development is well recognized, the molecular mechanisms controlling the transcriptional activity of GLI1 are poorly characterized. To identify regulatory components that participate in the transcriptional activity of GLI1, we explored GLI1 putative interacting proteins by liquid chromatography tandem mass spectrometry following immunoprecipitation of endogenous GLI1. We detected that the inhibitor of NF-KB kinase, IKKβ, is one of the proteins associated with GLI1 transcription factor. Here we investigate the regulatory role of IKKβ in the transcriptional activity of GLI1. We show that IKKβ regulates the transcriptional activity of GLI1 by phosphorylating GLI1 in C-terminal region and modulating its protein stability. Short stimulation of SUDHL4 and DOHH2 cells with TNF-α (20ng/mL) resulted in increased GLI1 protein levels. Similar results were observed in 293T cells transiently transfected with GLI1 and IKKβ kinase constructs. Moreover, silencing of IKKβ using siRNA and shRNAs led to decreased GLI1 protein levels and its transcriptional activity in DLBCL cell lines with constitutive activation of the NF-KB. Next, we characterized nine probable IKKβ dependent GLI1 phosphorylation sites (S543-S548, S1070, S1071 and S1074 identified by nanospray ion trap mass spectrometry) using mutational and deletions studies. We show that IKKβ phosphorylates GLI1 at Thr1074 and decreases binding between GLI1 and HECT-type E3 ubiquitin ligase (ITCH) resulting in reduced GLI1 polyubiquitination and degradation. Point mutation of Threonine 1074 to Alanine prevents IKKβ-mediated GLI1 phosphorylation and facilitates GLI1-ITCH interaction, polyubiquitination and degradation of GLI1 in the proteasome. Collectively, our data links IKKβ-mediated NF-kB signaling to the transcriptional activity of GLI1 and illustrates a novel cross talk between these two pathways. This is of clinical interest because activation of the NF-kB pathway is frequent in DLBCL and the connection between Hh and NF-kB pathways may open novel therapeutic avenues for DLBCL. Disclosures No relevant conflicts of interest to declare.
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Ggandison, Lindsey, Garry P. Nolan, and Donald W. Pfaff. "Activation of the transcription factor NF-KB in GH3 pituitary cells." Molecular and Cellular Endocrinology 106, no. 1-2 (December 1994): 9–15. http://dx.doi.org/10.1016/0303-7207(94)90180-5.

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Dissertations / Theses on the topic "Facteur de transcription NF-kB"

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Bottero, Virginie. "Dissection des mécanismes d'activation du facteur de transcription NF-KB." Nice, 2002. http://www.theses.fr/2002NICE5720.

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Derudder, Emmanuel. "Mécanismes de contrôle du facteur de transcription RelB, un membre de la famille NF-kB/Rel." Paris 6, 2003. http://www.theses.fr/2003PA066091.

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Charles, richard John lalith. "FACT, réparation par excision de bases et fixation du facteur de transcription NF-kB sur la chromatine." Phd thesis, Université de Grenoble, 2012. http://tel.archives-ouvertes.fr/tel-00770327.

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FACT est une protéine clé, qui joue de multiples rôles, y compris dans la transcription et la réparation de l'ADN endommagé. Néanmoins, comment FACT participe à la réparation et à la transcription de la chromatine n'est pas élucidé. Dans ce travail nous avons tout d'abord étudié le rôle de FACT dans le processus de réparation par excision de base (BER). Nous avons utilisé des nucléosomes reconstitués avec de l'ADN à uracile incorporé au hasard. Nous avons trouvé que l'enzyme UDG est capable d'enlever les uraciles localisés du côté de la solution et pas les uraciles se trouvant en face de l'octamère d'histone. La présence simultanée de FACT et de RSC (facteur de remodelage de la chromatine, impliqué dans la réparation) permet un enlèvement efficace des uraciles localisés du côté de l'octamère d'histone par l'UDG. De plus, l'action concertée de FACT et RSC contribue à l'enlèvement de la lésion oxidative 8-oxoG, autrement inaccessible, de la matrice nucléosomale par l'enzyme OGG1. Ce résultat est obtenu grâce à une activité " co-remodelatrice " de la protéine FACT. Dans ce travail nous décrivons pour la première fois cette nouvelle propriété de FACT et nous montrons par une série d'expériences biochimiques que FACT est capable de stimuler l'activité de remodelage du RSC. Nos expériences montrent que la présence de FACT augmente l'efficacité de RSC à transformer l'énergie libérée par l'hydrolyse de l'ATP en travail " mécanique ". Les données obtenues suggèrent une nature stochastique du BER in vivo, FACT étant un facteur clé dans le processus de réparation. Nous avons également investigué l'implication de l'activité co-remodelatrice de FACT dans la fixation de NF-kB aux matrices nucléosomales. La production de nucléosomes remodelés, mais non - mobilisés (remosomes) n'est pas suffisante pour promouvoir la fixation de NF-kB. Pourtant, la mobilisation des nucléosomes par l'intermédiaire de RSC permet une interaction efficace entre NF-kB et l'ADN nucléosomal. Toutes ces données sont essentielles pour le décryptage du mécanisme moléculaire par lequel FACT agit dans le BER et dans la transcription médiée par NF-kB.
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Charles, Richard John Lalith. "FACT, réparation par excision de bases et fixation du facteur de transcription NF-kB sur la chromatine." Thesis, Grenoble, 2012. http://www.theses.fr/2012GRENV034/document.

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FACT est une protéine clé, qui joue de multiples rôles, y compris dans la transcription et la réparation de l'ADN endommagé. Néanmoins, comment FACT participe à la réparation et à la transcription de la chromatine n'est pas élucidé. Dans ce travail nous avons tout d'abord étudié le rôle de FACT dans le processus de réparation par excision de base (BER). Nous avons utilisé des nucléosomes reconstitués avec de l'ADN à uracile incorporé au hasard. Nous avons trouvé que l'enzyme UDG est capable d'enlever les uraciles localisés du côté de la solution et pas les uraciles se trouvant en face de l'octamère d'histone. La présence simultanée de FACT et de RSC (facteur de remodelage de la chromatine, impliqué dans la réparation) permet un enlèvement efficace des uraciles localisés du côté de l'octamère d'histone par l'UDG. De plus, l'action concertée de FACT et RSC contribue à l'enlèvement de la lésion oxidative 8-oxoG, autrement inaccessible, de la matrice nucléosomale par l'enzyme OGG1. Ce résultat est obtenu grâce à une activité « co-remodelatrice » de la protéine FACT. Dans ce travail nous décrivons pour la première fois cette nouvelle propriété de FACT et nous montrons par une série d'expériences biochimiques que FACT est capable de stimuler l'activité de remodelage du RSC. Nos expériences montrent que la présence de FACT augmente l'efficacité de RSC à transformer l'énergie libérée par l'hydrolyse de l'ATP en travail « mécanique ». Les données obtenues suggèrent une nature stochastique du BER in vivo, FACT étant un facteur clé dans le processus de réparation. Nous avons également investigué l'implication de l'activité co-remodelatrice de FACT dans la fixation de NF-kB aux matrices nucléosomales. La production de nucléosomes remodelés, mais non - mobilisés (remosomes) n'est pas suffisante pour promouvoir la fixation de NF-kB. Pourtant, la mobilisation des nucléosomes par l'intermédiaire de RSC permet une interaction efficace entre NF-kB et l'ADN nucléosomal. Toutes ces données sont essentielles pour le décryptage du mécanisme moléculaire par lequel FACT agit dans le BER et dans la transcription médiée par NF-kB
FACT is a vital protein which has multiple roles including one in transcription and repair of damaged DNA. However, how FACT assists repair and transcription remains elusive. In this work, we have first studied the role of FACT in Base Excision Repair (BER). We used nucleosomes containing DNA with randomly incorporated uracil. We found that the enzyme UDG is able to remove uracils facing the solution and not the uracils facing the histone octamer. The simultaneous presence of FACT and RSC (a chromatin remodeler involved in repair) allows, however, a very efficient removal of uracil facing the histone octamer by UDG. In addition, the concerted action of FACT and RSC permits the removal of the otherwise un-accessible oxidative lesion 8-oxoG from nucleosomal templates by OGG1. This was achieved thanks to the co-remodeling activity of FACT. Here we described for the first time this novel property of FACT and we show in a series of biochemical experiments that FACT is able to boost the remodeling activity of RSC. The experiments reveal that the presence of FACT increases the efficiency of RSC to transform the energy freed by ATP hydrolysis into “mechanical” work. The presented data suggest a stochastic nature of BER functioning in vivo, FACT being a key factor in the repair process. The implication of the co-remodeling activity of FACT in NF-kB factor binding to nucleosomal templates was also investigated. The generation of remodeled, but not mobilized nucleosomes (remosomes), was not sufficient to promote NF-kB binding. However, the RSC-induced nucleosome mobilization allows efficient NF-kB interaction with nucleosomal DNA. Our data are instrumental in deciphering the molecular mechanism of FACT implication in BER and NF-kB mediated transcription
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VALLEE, SEBASTIEN. "Role du facteur de transcription nf-kb dans la survie et la differenciation de la cellule tumorale." Paris 11, 2001. http://www.theses.fr/2001PA112079.

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Nf-kb est un facteur de transcription regissant de nombreux mecanismes cellulaires, il est preponderant dans les phenomenes inflammatoires. Il regule positivement ou le plus souvent negativement l'apoptose suivant le type cellulaire. Cet effet l'impliquerait dans la progression tumorale des adenocarcinomes. Ce facteur intervient egalement dans les pathologies inflammatoires du tube digestif. Dans une 1 e r e partie, nous mettons en evidence une dualite des effets de l'igf-1 sur le controle de genes portant le site kb : l'igf-1 inhibe la degradation de ikb, l'inhibiteur naturel de nf-kb et freine la translocation de nf-kb, alors qu'il potentialise la transcription du gene de l'il-8 dont l'expression est dependante de nf-kb. Dans une 2 e m e partie, nous avons etudie les mecanismes d'activation de nf-kb par l'il-1, une cytokine pro-inflammatoire. Dans les cellules ht29-d4 non differenciees, on observe une perte d'activation de nf-kb en reponse a l'il-1. Cette perte est correlee avec l'absence de translocation subcellulaire de la pkc. L'activation de nf-kb dependante de l'il-1 est restauree lorsque les cellules ht29-d4 se differencient. De plus, la translocation des pkc est egalement restauree et l'inhibition des pkc bloque l'activation de nf-kb. Ces changements au niveau de la voie de signalisation regulee par l'il-1 pourraient etre lies a une modification dans l'etat du cytosquelette intervenant dans la dedifferenciation cellulaire car la translocation des pkc est dependante de la structure du cytosquelette. Dans la 3eme partie, en comparant deux types cellulaires ht29-d4 et hbl 100, nous avons montre l'existence d'une correlation entre la depolymerisation des microtubules par des agents depolymerisants, l'activation de nf-kb
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Laguillier, Christelle. "Inhibition spécifique de facteurs de transcription impliqués dans la cancérogenèse : application à NF-KB et STAT3." Paris 7, 2008. http://www.theses.fr/2008PA077122.

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L'émergence de tumeurs résulte de la dérégulation de plusieurs fonctions cellulaires, dont les voies impliquant des facteurs transcriptionnels (FTs) clés comme NF-KB et STAT3. L'objectif du travail était l'étude des effets et des mécanismes d'action d'inhibiteurs spécifiques de ces FTs dans des lignées tumorales. L'expression d'un dominant négatif mute�� de I-KB dans des lignées de lymphocytes B, entraîne une diminution de l'activité de NF-KB et sensibilise les cellules à l'apoptose induite par le TNFα. En revanche, l'inactivation du TNFa par un anticorps monoclonal est sans effet. Les oligonucléotides-leurres (ODNs) peuvent inhiber spécifiquement les FTs en bloquant leur domaine de liaison à l'ADN, ils empêchent ainsi la transcription de leurs gènes cibles. Un ODN, en épingle à cheveux, s'est révélé efficace pour bloquer spécifiquement NF-KB dans le cytoplasme de lignées cellulaires dérivées d'un cancer colorectal (SW480) et d'un cancer mammaire (MCF7), induisant ainsi l'apoptose. Nous avons obtenu des résultats similaires dans les cellules SW480 avec un ODN en épingle à cheveux dirigé contre STAT3. Mais, cet ODN inhibe aussi STAT1 activé protégeant les cellules contre la mort induite par l'interféron y. Cela montre l'importance de l'équilibre entre les formes actives de STAT1 et STAT3 dans l'évolution des cellules SW480 vers la survie ou vers la mort. Nos travaux montrent que l'inhibition spécifique par des ODNs, de FTs impliqués dans la prolifération cellulaire permet d'induire l'apoptose des cellules des lignées tumorales dans lesquelles ces FTs sont activés. La modélisation moléculaire devrait permettre d'augmenter la spécificité des ODNs pour leur cible
The growth of tumour cells results in part from deregulation of several cellular functions, including that of pathways involving key transcriptionnal factors (TFs) such as NF-KB or STAT3. In this work we studied the effects and the mechanism of action of specific inhibitors of NF-KB and STAT3 in tumour cell lines. By expressing a mutated form of I-LB in B cell lines, we observed a decreased NF-KB activity and increased induction of apoptosis by TNFα , on the other hand an antibody to TNFa had no direct effect on these cells. Decoy oligonucleotides (decoy ODN) allow the specific inhibition of the TFs by interacting with their DNA binding region. An NF-KB hairpin decoy ODN specifically blocked NF-KB in a colorectal cancer cell line (SW480) and in a mammary cancer cell line (MCF7), thereby inducing apoptosis of these cells. We obtained identical results in the SW480 cells with a STAT3 hairpin decoy ODN. Interestingly, this decoy ODN also inhibited interferony-activated STAT1 resulting in the protection of the cells against interferony-induced apoptosis. These results suggest that a balance between the levels of activated STAT1 and activated STAT3 play a role in the orientation of the SW480 cells toward proliferation or cell death. Thus, targeting TFs involved in cell proliferation with ODNs can efficiently inhibit them and induce the death of the cancer cell lines in which they are activated. Molecular modelling should allow to increase the specificity of the decoy ODNs for their target
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Ben, Ameur Lamya. "Rôle de l’activation chronique de la voie NF-kB induite par l’oncoprotéine Tax du virus HTLV-1 dans la régulation de l’épissage alternatif." Thesis, Lyon, 2019. http://www.theses.fr/2019LYSE1136.

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La voie de signalisation NF-kB (nuclear factor kB) régule la transcription de gènes impliqués dans la réponse immune et l’inflammation. L’activation chronique de cette voie est fréquemment retrouvée associée à des désordres inflammatoires et des cancers. Les impacts fonctionnels de l’activation de la voie NF-kB ont été jusqu’à présent étudiés à l’échelle des promoteurs. Néanmoins, les études récentes de la distribution chromatinienne de NF-kB indiquent que la sous-unité NF-kB RelA se localise majoritairement dans les régions intragéniques, incluant des exons et des introns, où ses fonctions restent inconnues. Mes travaux ont consisté à adresser cette question dans le contexte de l’infection par le virus HTLV-1, un activateur chronique de la voie NF-kB, responsable de la leucémie T de l’adulte. Mes données montrent que l’activation de la voie NF-kB par l’oncogène viral Tax de HTLV-1 s’accompagne de modifications de l’épissage alternatif d’exons riches en GC qui coïncident avec le recrutement chromatinien de RelA à proximité de ces exons régulés. Les analyses intégratives des profils d’épissage et du remodelage de la chromatine, combinées à des essais de ciblage expérimental de la chromatine (TALE), démontrent que la fixation intragénique de RelA permet de recruter le régulateur d'épissage DDX17 pour moduler l’épissage alternatif de l’exon via son activité hélicase. Ces données révèlent que, outre ses fonctions transcriptionnelles, le facteur NF-kB RelA agit comme une ancre chromatinienne pour le facteur d’épissage DDX17 et fournit une spécificité de régulation d’épissage alternatif. Ces données revisitent nos connaissances des mécanismes physiopathologiques des maladies associées à HTLV-1 ainsi que d'autres désordres reliés à l’activation chronique de la voie NF-kB
The NF-kB (nuclear factor kB) signaling pathway regulates gene transcription of genes involved in immune response and inflammation. Chronic activation of NF-kB frequently associated with inflammatory disorders and cancer. The functional impacts of NF-kB have long been studied at the promoter level. Nevertheless, recent studies of the chromatin distribution of RelA indicate that this NF-kB subunit is predominantly localized in intragenic regions, including exons and introns, where its functions remain unknown. My work has addressed this question in the context of HTLV-1 infection, which is a constitutive activator of NF-kB, and the causative agent of the Adult T-cell Leukemia. The results show that the activation of NF-kB by the viral oncoprotein Tax results in changes in alternative splicing regulations of GC-rich exons that coincide with the chromatin recruitment of RelA in the vicinity of these exons. Integrative analysis of RNA splicing and chromatin occupancy, combined with experimental chromatin tethering assays (TALE) demonstrate that the intragenic binding of RelA leads to the recruitment of the splicing regulator DDX17, which modulates the inclusion rate of exon thanks to its helicase activity. Altogether, these data reveal that, besides its transcriptional role, NF-kB RelA acts as a chromatin anchor for the splicing factor DDX17 and provides alternative splicing specificity. These data revisit our knowledge of the physiopathologic mechanisms of HTLV-1 associated diseases , as well as other disorders related to the chronic activation of the NF-kB pathway
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Kfoury, Youmna. "Mécanismes moléculaires de l'activation de la voie NF-KB par l'oncoprotéine virale d'HTLV-1 : Tax." Paris 7, 2010. http://www.theses.fr/2010PA077022.

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Le virus humain lymphotrope de type-1 (HTLV-I) est lié à plusieurs pathologies humaines comme la Leucémie T de l'adulte et la paraparésie spastique tropicale ou myélopathie associée à HTLV-1 (TSP/HAM). L'activation de la voie NF-KB par l'oncoprotéine virale Tax joue un rôle clé dans l'induction et le maintien de la prolifération cellulaire ainsi que l'inhibition de l'apoptose. Les modifications post-traductionnelles de Tax par Pubiquitylation et la SUMOylation sont impliquées dans l'activation de la voie NF-KB, mais les mécanismes moléculaires qui gouvernent cette activation restent assez mal compris. Nous avons montré que Tax ubiquitylée n'est pas associée avec l'IKK active dans le cytoplasme mais qu'elle se lie avec les trois sous-unités d'IKK et les cible dans le centrosome. En fait Tax est différentiellement ubiquitylée : Tax ubiquitylée avec des chaînes K-48 est destinée à la dégradation par le protéasome et est ainsi stabilisée en présence de l'inhibiteur du protéasome PS-341, alors que Tax ubiquitylée avec des chaînes K-63 se localise dans le centrosome avec IKK-y, puis recrute IKK-α et IKK-β. Le centrosome constitue ainsi la plateforme d'interaction entre Tax et IKK. Nous avons également montré que la même molécule de Tax fait le trafic entre des corps nucléaires Ubc9 et le centrosome. En fait, Pubiquitylation de Tax cible Tax et NEMO dans des corps Ubc9 riches en SUMO. Par ailleurs, Tax induit la SUMOylation et le ciblage nucléaire de NEMO. En somme, nous avons montré que Pubiquitylation et la SUMOylation de Tax contrôlent le trafic bidirectionnel et dynamique de Tax et NEMO entre les corps nucléaires Ubc9 et le centrosome
The human T-lymphotropic virus type-1 (HTLV-I) is associated with several human pathologies such as adult T-cell leukemia/lymphoma and tropical spastic paraparesis/HTLV-I associated myelopathy. NF-Kβ activation by the viral oncoprotein Tax plays a crucial role in the induction and maintenance of cellular proliferation and inhibition of apoptosis. Tax post-translational modification by ubiquitylation and SUMOylation is involved in NF-KB activation but the molecular mechanisms underlying this activation remain unclear. We showed that ubiquitylated Tax does not interact with active IKK in the cytoplasm but binds the three IKK subunits and targets them to the centrosome. Actually, Tax is differentially ubiquitylated: K-48 ubiquitylated Tax is destined for proteasomal degradation and is stabilized upon treatment with the proteasome inhibitor PS-341. On the other hand, K-63 ubiquitylated Tax colocalizes with IKK-y in the centrosome where IKK-α and IKK-β are also recruited. Hence, the centrosome represents the platform for Tax/IKK interaction. We also showed that the same Tax molecules shuttle between Ubc9 nuclear bodies and the centrosome. Indeed, Tax ubiquitylation targets Tax and NEMO into Ubc9- and SUMO- rich nuclear bodies. Moreover, Tax induces NEMO SUMOylation and accumulation in the nuclear fraction. In conclusion, Tax ubiquitylation and SUMOylation control the bidirectional and dynamic trafficking of Tax and NEMO between the Ubc9 nuclear bodies and the centrosome
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Poalas, Konstantinos. "Ubiquitinylation and deubiquitinylation in the regulation of the transcription factor NF-kB activation." Phd thesis, Université Paris Sud - Paris XI, 2013. http://tel.archives-ouvertes.fr/tel-00926894.

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Large signalosome assembly is a prerequisite for NF-κB signaling upon engagement of various immunoreceptors. Adaptor proteins containing protein-protein interaction domains oligomerise in response to such stimuli in order to propagate signaling. Each immunoreceptor uses distinct adaptors, as well as common ones, to achieve that. The main characteristic shared by these proteins is their ability to undergo poly-ubiquitinylation in a non-degradative manner, leading to optimal NF-κB activation. In this work, we aimed to identify novel deubiquitinylating enzymes that control ubiquitinylation status. That is how USP34 came up to be a negative regulator of NF-κB signaling in TCR-activated Jurkat cells, a T lymphocyte cell line. Our data suggest a model whereby USP34 prevents excessive NF-κB activation by acting rather late, directly or indirectly on the NF-κB:IκBα dimers, downstream of IKK, altering transcription factor DNA binding affinity. In parallel, studies of the endocellular membrane microenvironment that hosts mature signalosomes in response to TCR-, TNFR- and CD40 ligation led to the identification of an ER-residing protein, Metadherin (MTDH), which seems to globally integrate signaling before forwarding it to downstream pathway components able to activate IKK.
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Roy, Evelyne. "Modulation de la réponse inflammatoire intestinale par la kinase DNA-PK." Mémoire, Université de Sherbrooke, 2007. http://savoirs.usherbrooke.ca/handle/11143/3931.

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Des résultats obtenus antérieurement au laboratoire ont démontré l'induction des facteurs de transcription C/EBPs par l'IL-1? ainsi que leur implication dans la régulation de la transcription de gènes de réponse inflammatoire telle que l'haptoglobine au niveau de la cellule épithéliale intestinale. En outre, il a déjà été démontré que la phosphoiylation des C/EBPs peut moduler leur activité et des études au laboratoire ont démontré l'interaction in vitro entre l'isoforme C/EBP? et la kinase DNA-PK. Par l'utilisation de l'inhibiteur non spécifique de la famille PI(3)K, la wortmannine, il a été observé que la DNA-PK phosphoryle C/EBP?. La DNA-PK est une kinase qui répare les bris d'ADN double brin en participant au processus de jonction des extrémités non-homologues. Ainsi, nous avons étudié la modulation de la réponse inflammatoire intestinale par la DNA-PK, en s'attardant plus particulièrement à deux familles de facteurs de transcription, soit NF-?B et les C/EBPs. Par l'utilisation d'un inhibiteur sélectif de la DNA-PK, le IC60211, la phosphorylation in vitro de la région N-terminale de C/EBP? par la DNA-PK a d'abord été confirmé. Puisque la DNA-PK est activée par les bris d'ADN double brin, la doxorubicine, un agent génotoxique, a été utilisé pour la suite du projet. Nous avons montré que la doxorubicine engendre une hausse de la capacité de liaison à l'ADN de NF-?B induite par l'IL-1? et que les complexes formés comprenaient surtout la sousunité p65. Ceci s'accompagne d'une hausse des niveaux nucléaires de p65 ainsi que d'une baisse d'expression de l'inhibiteur cytoplasmique de NF-?B, I?B?. Par contre, par l'utilisation de l'inhibiteur sélectif de la DNA-PK, le NU7026, nos résultats suggèrent que ces effets sont DNA-PK indépendants. En effet, un rétablissement de la capacité de liaison à l'ADN de NF-?B n'est pas observé lors d'une préincubation avec cet inhibiteur avant de traiter à la doxorubicine puis à l'IL-1?. En ce qui concerne les C/EBPs, nos résultats démontrent que la doxorubicine diminue l'activité transcriptionnelle de l'isoforme C/EBP? sur le promoteur du gène haptoglobine. Alors qu'un traitement à l'IL-1? induit une augmentation de la liaison des C/EBPs à HaptoA, nos résultats montrent qu'un pré-traitement à la doxorubicine empêche cette induction. De plus, les niveaux protéiques de C/EBP? et C/EBP? induits par l'IL-1? sont abaissés par la doxorubicine. Également, les niveaux d'ARNm de C/EBP? induits par l'IL-1 p et de deux de ses gènes cibles inflammatoires, l'haptoglobine et lipocalin2, sont diminués par un prétraitement à la doxorubicine. Par l'utilisation du NU7026, nous démontrons un rétablissement partiel de la capacité de liaison à l'ADN de C/EB13? et de C/EBP? qui était réduite par un traitement à la doxorubicine, à des niveaux comparables à la condition sans traitement et à la condition IL-1?, respectivement. Cependant, cet inhibiteur permet le rétablissement des niveaux de protéine et d'ARNm de C/EBP? (induits par l'IL-1?) qui étaient réprimés par un prétraitement à la doxorubicine mais non des niveaux protéiques de C/EBP?. Nos résultats suggèrent que la DNA-PK régule, au moins partiellement, la transcription de l'isoforme C/EBP? ainsi que son activité transcriptionnelle sur le promoteur de l'haptoglobine. Par contre, nos résultats suggèrent aussi que la DNA-PK module la capacité de liaison à l'ADN de C/EBP? et que l'effondrement des niveaux protéiques de C/EBP? par la doxorubicine est DNA-PK indépendant. [Symboles non conformes]
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Books on the topic "Facteur de transcription NF-kB"

1

Liou, Hsiou-Chi. NF-kB/Rel transcription factor family. Georgetown, TX: Landes Bioscience/Eurekah.com, 2006.

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Liou, Hsiou-Chi, ed. NF-κB/Rel Transcription Factor Family. Boston, MA: Springer US, 2006. http://dx.doi.org/10.1007/0-387-33573-0.

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Liou, Hsiou-Chi. Nf-kb/rel Transcription Factor Family. Eurekah.Com Inc, 2005.

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NF-kB/Rel Transcription Factor Family (Molecular Biology Intelligence Unit). Springer, 2007.

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Handbook of Transcription Factor NF-kappaB. CRC, 2006.

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Ghosh, Sankar. Handbook of Transcription Factor NF-KappaB. Taylor & Francis Group, 2006.

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Hsiou-Chi, Liou, ed. NF-[kappa]B/Rel transcription factor family. Georgetown, Tex: Landes Bioscience/Eurekah.com, 2006.

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Su, Ming. Nuclear factor Y (NF-Y) mediated regulation of bone sialoprotein (bsp) gene transcription through an inverted CCAAT box. 2006.

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Book chapters on the topic "Facteur de transcription NF-kB"

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Gumina, Stefano. "The Possible Role of the Transcription Factor NF-kB on Evolution of Rotator Cuff Tear and on Mechanisms of Cuff Tendon Healing." In Rotator Cuff Tear, 213–19. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-33355-7_27.

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Loop, T., and H. L. Pahl. "Activators and Target Genes of Rel/NF-кB Transcription Factors." In Nuclear Factor кB, 1–48. Dordrecht: Springer Netherlands, 2003. http://dx.doi.org/10.1007/978-94-010-0163-2_1.

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Pepper, Chris, and Chris Fegan. "Chapter 5. Small Molecule Inhibitors of NF-κB and Their Therapeutic Potential in Leukaemia." In Small-molecule Transcription Factor Inhibitors in Oncology, 125–46. Cambridge: Royal Society of Chemistry, 2018. http://dx.doi.org/10.1039/9781782624011-00125.

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Ghosh, Gourisankar, De-Bin Huang, and Tom Huxford. "Recognition of Nucleic Acids by Transcription Factor NF-κB." In Biological and Medical Physics, Biomedical Engineering, 85–106. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-0-387-92808-1_5.

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Chen, Fei, and Xianglin Shi. "NF-кB, a pivotal transcription factor in silica-induced diseases." In Oxygen/Nitrogen Radicals: Cell Injury and Disease, 169–76. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4615-1087-1_19.

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Piette, Jacques. "Importance of Trace Elements in Transcription Factor NF-κB Activation." In Trace Elements in Man and Animals 10, 89–96. New York, NY: Springer US, 2002. http://dx.doi.org/10.1007/0-306-47466-2_18.

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Bours, V., G. Franzoso, K. Brown, S. Park, V. Azarenko, M. Tomita-Yamaguchi, K. Kelly, and U. Siebenlist. "Lymphocyte Activation and the Family of NF-κB Transcription Factor Complexes." In Current Topics in Microbiology and Immunology, 411–20. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-77633-5_52.

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Brasier, Allan R., M. Jamaluddin, Youqi Han, Cam Patterson, and Marschall S. Runge. "Angiotensin II induces gene transcription through cell-type-dependent effects on the nuclear factor-кB (NF-кB) transcription factor." In Control of Gene Expression by Catecholamines and the Renin-Angiotensin System, 155–69. Boston, MA: Springer US, 2000. http://dx.doi.org/10.1007/978-1-4615-4351-0_18.

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Mauro, Claudio, Francesca Zazzeroni, Salvatore Papa, Concetta Bubici, and Guido Franzoso. "The NF-κB Transcription Factor Pathway as a Therapeutic Target in Cancer: Methods for Detection of NF-κB Activity." In Methods in Molecular Biology™, 169–207. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-530-9_10.

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Muraoka, Kei-ichi, Xiangao Sun, Tetuhiko Go, You Watanabe, and Ken-ichi Yamamoto. "Effects of Natural Antioxidants on the Activation of Transcription Factor NF-κB and p53." In Food Factors for Cancer Prevention, 468–71. Tokyo: Springer Japan, 1997. http://dx.doi.org/10.1007/978-4-431-67017-9_92.

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Conference papers on the topic "Facteur de transcription NF-kB"

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Вульф, Мария Александровна, Дарья Александровна Скуратовская, Александра Андреевна Комар, and Лариса Сергеевна Литвинова. "AMPK AND SIRT1 IN THE REGULATION OF LIVER METABOLISM IN OBESE PATIENTS WITH TYPE 2 DIABETES MELLITUS." In Наука. Исследования. Практика: сборник избранных статей по материалам Международной научной конференции (Санкт-Петербург, Декабрь 2020). Crossref, 2021. http://dx.doi.org/10.37539/srp294.2020.80.71.015.

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У больных ожирением выявлены взаимосвязи основных регуляторов метаболизма (AMPK и SITRT1) в печени с нарушениями со стороны липидного и углеводного обменов. Установлена протекторная роль SIRT1 в подавлении экспрессии транскрипционного фактора NF-kB в печени, способствующего переходу стеатоза в стеатогепатит. In obese patients, interrelations of the main regulators of metabolism (AMPK and SITRT1) in the liver with lipid and carbohydrate metabolism disorders were revealed. The protective role of SIRT1 in suppressing the expression of the transcription factor NF-kB in the liver, which promotes the transition of steatosis to steatohepatitis, has been established.
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Wolfe, Valerie M., Seonghun Park, Marjana Tomic, Peter A. Torzilli, and C. T. Christopher Chen. "Load Down-Regulates TNF-Alpha Induced Cartilage Degradation in Part Through NF-KB and P38 Pathways." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176541.

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Pro-inflammatory cytokines, such as interleukin-1 (IL-1) and tumor necrosis factor (TNF), can induce cartilage degradation after acute injury or in inflammatory diseases [1,2,3,7]. The degradative events are coordinated through the elevation and activation of two classes of enzymes, namely matrix metalloproteinases (MMPs) and aggrecanases (ADAMTS-4 and −5) [1,6]. Prior studies suggested that pro-inflammatory responses induced by IL-1β can be inhibited by tensile load [2] and more recently by cyclic compression [8]. It is, however, not clear whether load affects other cytokines, such as TNF-α. TNF-α is known to bind its receptor (TNFR1) to cause a cascade that ends with degradation of an inhibitor, IκBα, and release of the transcription factor NF-κB [3]. The actions of TNF-α are also known to be affected by at least three NF-κB independent pathways including the p38, ERK, and JNK pathways [4]. The objective of this study was to determine whether cyclic compression could affect TNF-α induced cartilage degradation and to determine the roles of p38, ERK, and JNK pathways in TNF-induced cartilage degradation. We hypothesized that cyclic loading would inhibit the degradative effects caused by TNF-α.
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Hussain, Showket, Neha Singh, Irfana Salam, Mohammad A. Bhat, Nandita Kakkar, Mohammad M. Mir, Mushtaq A. Siddiqi, et al. "Abstract 2722: Transcription factor NF-kB in esophageal squamous cell carcinoma: Alterations in activity and expression during Human Papillomavirus infection." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-2722.

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4

Jayaraman, Swaathi, Mary J. Kuffel, Krishna R. Kalari, Kevin J. Thompson, Xiaojia Tang, Elizabeth S. Bruinsma, John R. Hawse, and Matthew P. Goetz. "Abstract P6-04-06: Protein kinase C beta 1 (PKCβ1), a novel drug target of Z-endoxifen, inhibits growth of estrogen receptor positive (ER+) breast cancer via activation of the NF-kB transcription factor RelA." In Abstracts: 2019 San Antonio Breast Cancer Symposium; December 10-14, 2019; San Antonio, Texas. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.sabcs19-p6-04-06.

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Collins, Corolyn J., Richard B. Levene, Christina P. Ravera, Marker J. Dombalagian, David M. Livingston, and Dennis C. Lynch. "MOLECULAR CLONING OF THE HUMAN GENE FOR VON WILLEBRAND FACTOR AND IDENTIFICATION OF THE TRANSCRIPTION INITIATION SITE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642830.

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Most patients with von Willebrand's disease appear to have a defect affecting the level of expression of the von Willebrand factor (vWf) gene. Thus, an understanding of the pathogenesis of von Willebrand's disease will require an analysis of the structure and function of the vWf gene in normals and in patients. To begin such analyses, we have screened a human genomic cosmid library with probes obtained from vWf cDNA and isolated a colinear segment spanning ≈175 kb in five overlapping clones. This segment extends ≈25 kb upstream and ≈5 kb downstream of the transcription start and stop sites for vWf mRNA, implying the vWf gene has a length of ≈150 kb. Within one of these clones, the vWf transcription initiation sites have been mapped. A portion of the promoter region has been sequenced, revealing a typical TATA box, a downstream CCAAT box, and a perfect downstream repeat of the 8 base pairs containing the major transcription start site. Primer extension analysis suggests that sequences contained within the downstream repeat of the transcription start site may be used as minor initiation sites in endothelial cells. Transfection studies are underway to evaluate the role of sequences within this promoter region in gene regulatory activity. Comparative restriction analyses of cloned and chromosomal DNA segments strongly suggests that no major alterations ocurred during cloning and that there is only one complete copy of the vWf gene in the human haploid genome. Similar analyses of DNA from vWf-expressing endothelial cells and non-expressing white blood cells suggests that no major rearrangements are associated with vWf gene expression. Finally, cross hybridization patterns among seven mammalian species suggests a strong conservation of genomic sequences encoding the plasma portion of vWf, but a lower degree of conservation of sequences encoding the N terminal region of provWf.
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Bisio, Alessandra, Judit Zámborszky, Sara Zaccara, Mattia Lion, Toma Tebaldi, Yari Ciribilli, and Alberto Inga. "Abstract 746: Functional crosstalk between the p53 and NF-kB transcription factors." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-746.

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Wu, Q. Y., B. R. Bahnak, L. Coulombel, J. P. Caen, G. Pietu, and D. Meyer. "VON WILLEBRAND FACTOR mRNA IS SEVERELY REDUCED IN PIGS WITH HOMOZYGOUS VON WILLEBRAND DISEASE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644113.

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Porcine von Willebrand disease (vWD), an autosomal recessive disorder, is similar to some of the severe forms of vWD in humans and is characterized by a prolonged bleeding time and very low or undetectable amounts of von Willebrand factor (vWF) antigen and activity in plasma, platelets and endothelial cells. The molecular events that control the lack of expression of vWF in the vWD pigs is not known and could be at the transcriptional or post-transcriptional level. Lungs from normal and two homozygous vWD pigs were extracted immediately after harvesting of the animals and placed on dry ice. Tissues were homogenized in 6 M guanidinium thiocyanate and RNA isolated by centrifugation through cesium chloride. Total RNA was analyzed by Northern hybridization including dénaturation in glyoxal, electrophoresis in 1.0 % agarose-2.2 M formaldehyde gels and transfer onto nitrocellulose. Messenger RNA was detected with a nick-translated human vWF cDNA probe or a human actin control probe. The vWF probe, cloned from a human lung library, was 2,280 bp in length and spanned nucleotides 960 to 3,240 of the human cDNA. These human probes were considered valid to detect levels of porcine vWF and actin mRNA because they hybridized with restriction enzyme digested genomic DNA from normal and vWD pig leucocytes under conditions of high stringency. The size of the vWF mRNA in the normal pigs after Northern hybridization was approximately 9.0 kb, similar to that of human vWF mRNA, and was easily detectable at the lowest concentration of RNA blotted (5 ug). In contrast, vWF mRNA from vWD pigs was at the lower limit of detection even at 10 ug of total RNA blotted. Nevertheless, although at extremely low levels, vWF mRNA from vWD pigs appeared to be the same size as the normal mRNA. These results agree with observations on the relationship of vWF secreted from 24 hr. cultures of endothelial cells from the pulmonary artery of normal and vWD pigs where the vWF levels were 0.90 and 0.06 U/108 cells, respectively. Therefore, it appears that the very low expression of vWF in the vWD pigs is due to a lack of transcription of the vWF gene. At this time, however, turnover of unstable transcripts in the vWD pigs can not be ruled out.
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Schmidt, Christopher R., Christopher C. Oakes, Michael Boutros, and Christoph Plass. "Abstract 2180: Identification of nuclear transcription factor Y (NF-Y) as a novel key transcriptional regulator of the tumor-suppressor geneDAPK1." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-2180.

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Agarwal, Nitin K., Kranthi Kunkalla, and Francisco Vega. "Abstract 3605: The inhibitor of NF-ĸB kinase, IKKβ, regulates the stability of GLI1 transcription factor." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-3605.

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Marquerie, G., A. Duperray, G. Uzan, and R. Berthier. "BIOSYNTHETIC PATHWAYS OF THE PLATELET FIBRINOGEN RECEPTOR IN HUMAN MEGAKARYOCYTES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642954.

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Interaction between cells and between cells and extracellular matrices are critical for a number of biological processes, including organ development, cell differenciation, cell motility, and the inimune' response. These interactions are mediated by a family of adhesion receptors that recognize short sequences such as Arg-Gly-Asp (RGD). These receptors share similar structural properties. They are heterodimers composed of a and B subunits and sometime express common epitopes. This suggests that the structural and functional relationship of these receptors may result from the transcription of related genes or may arise from cell specific post-transcriptional events. Thus, analysis of the biosynthesis and processing of these receptors would provide valuable insights into the molecular mechanism which control their expression at the surface,of different cells. Platelet membrane glycoprotein (GP) IIb-IIIa is a member of this receptor family. This protein is a non covalent heterodimer composed of two distinct polypeptides, Glib which consists of two subunits Ilba and IlbB (Mr = 116 kD, Mr = 25 kD) and GPIIIa (Mr = 100 kD, reduced). GPIIb-IIIa functions at site of platelet aggregation and serves as receptor for RGD containing factors including fibrinogen, fibronectin and von Willebrand factor. We report here on the investigation of the biosynthetic pathways of this RGD receptor in human megakaryocytes. High number of megakaryocytic cells from the megakaryoblastic stage to the polyploid mature megakaryocyte were obtained from liquid culture of cryopreserved leukocyte stem cell concentrates from patients with chronic myelogenous leukemia (CML). After sorting, using a FACS IV and indirect immunofluores-cent labeling with monoclonal antibodies anti-GPIIb-IIIa, 95 % of the cells in culture were of the megakaryocytic lineage. These megakarocytes represented an excellent tool to delineate at the molecular level events associated with the biosynthesis of GPIIb-IIIa.Metabolic labeling and pulse-chase experiments indicated that GPIIb and GPIIIa are synthesized from separate mRNA and that the two subunits of GPIIb derive from a common precursor. This was further confirmed by cell-free translation of megakaryocyte mRNA and the identification of separate cDNA containing sequences coding for the pro-GPIIb and for GPIIIa. These cDNA were isolated from a Xgt11 expression library constructed with purified megakaryocyte RNA, and were used to size the messengers coding for the two polypeptides. A single mRNA species of 3.9 kB was found to encode the pro-GPIIb, whereas two different mRNA species of 2.9 kB and 4. 1 kB were identified with the GPIIIa cDNA.The newly synthesized GPIIIa associates early with the pro-GPIIb in the rough endoplasmic reticulum. Examination of the glycosylation pathways with endoglycosidase H, tunicamycin and monensin indicated that high mannose oligosaccharides are added to the GPIIIa and pro-GPIIb polypeptide backbone. The pro-GPIIb is then processed with conversion of high mannose to the complex type carbohydrate, whereas GPIIIa remains endoH sensitive. Glycosylation of pro-GPIIb-IIIa and processing of oligosaccharides are prerequisite for proteolytic maturation of pro-GPIIb and the expression of the mature complex at the surface of the cell. Thus post-translational processing of GPIIb-IIIa requires an early assembly of the complex. This may have important implications in the maturation of megakaryocyte granules and in the molecular mechanism underlying the Glanzmann thrombastenic disease.
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Reports on the topic "Facteur de transcription NF-kB"

1

Budunova, Irina V. Role of IKKs and Transcription Factor NF-kB in Prostate Tumorigenesis. Fort Belvoir, VA: Defense Technical Information Center, May 2003. http://dx.doi.org/10.21236/ada417764.

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Budunova, Irina V. Role of IKKs and Transcription Factor NF-kB in Prostate Tumorigenesis. Fort Belvoir, VA: Defense Technical Information Center, May 2002. http://dx.doi.org/10.21236/ada405665.

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3

Baldwin, Albert S. A Role for the NF-kB/Rel Transcription Factors in Human Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 1995. http://dx.doi.org/10.21236/ada300265.

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