Littérature scientifique sur le sujet « Oncoproteina Tax »
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Articles de revues sur le sujet "Oncoproteina Tax"
Heym, Stefanie, Caroline Mohr, Hanna Engelbrecht, Bernhard Fleckenstein et Andrea Thoma-Kress. « Alternative NF-κB Signaling Discriminates Induction of the Tumor Marker Fascin by the Viral Oncoproteins Tax-1 and Tax-2 of Human T-Cell Leukemia Viruses ». Cancers 14, no 3 (21 janvier 2022) : 537. http://dx.doi.org/10.3390/cancers14030537.
Texte intégralKress, Andrea K., Martina Kalmer, Aileen G. Rowan, Ralph Grassmann et Bernhard Fleckenstein. « The tumor marker Fascin is strongly induced by the Tax oncoprotein of HTLV-1 through NF-κB signals ». Blood 117, no 13 (31 mars 2011) : 3609–12. http://dx.doi.org/10.1182/blood-2010-09-305805.
Texte intégralNasr, Rihab, Estelle Chiari, Marwan El-Sabban, Renaud Mahieux, Youmna Kfoury, Mohammad M. Abdulhay, Olivier Hermine, Hugues de Thé, Claudine Pique et Ali Bazarbachi. « Tax Ubiquitylation and Sumoylation Control the Two Distinct Steps of NF-κB Activation. » Blood 106, no 11 (16 novembre 2005) : 4353. http://dx.doi.org/10.1182/blood.v106.11.4353.4353.
Texte intégralTwizere, Jean-Claude, Jean-Yves Springael, Mathieu Boxus, Arsène Burny, Franck Dequiedt, Jean-François Dewulf, Julie Duchateau et al. « Human T-cell leukemia virus type-1 Tax oncoprotein regulates G-protein signaling ». Blood 109, no 3 (21 septembre 2006) : 1051–60. http://dx.doi.org/10.1182/blood-2006-06-026781.
Texte intégralHaller, Kerstin, Yalin Wu, Elisabeth Derow, Iris Schmitt, Kuan-Teh Jeang et Ralph Grassmann. « Physical Interaction of Human T-Cell Leukemia Virus Type 1 Tax with Cyclin-Dependent Kinase 4 Stimulates the Phosphorylation of Retinoblastoma Protein ». Molecular and Cellular Biology 22, no 10 (15 mai 2002) : 3327–38. http://dx.doi.org/10.1128/mcb.22.10.3327-3338.2002.
Texte intégralFryrear, Kimberly A., Xin Guo, Oliver Kerscher et O. John Semmes. « The Sumo-targeted ubiquitin ligase RNF4 regulates the localization and function of the HTLV-1 oncoprotein Tax ». Blood 119, no 5 (2 février 2012) : 1173–81. http://dx.doi.org/10.1182/blood-2011-06-358564.
Texte intégralDucu, Razvan I., Tajhal Dayaram et Susan J. Marriott. « The HTLV-1 Tax oncoprotein represses Ku80 gene expression ». Virology 416, no 1-2 (juillet 2011) : 1–8. http://dx.doi.org/10.1016/j.virol.2011.04.012.
Texte intégralWu, Xuefeng, Minying Zhang et Shao-Cong Sun. « Mutual regulation between deubiquitinase CYLD and retroviral oncoprotein Tax ». Cell & ; Bioscience 1, no 1 (2011) : 27. http://dx.doi.org/10.1186/2045-3701-1-27.
Texte intégralReilly, Patrick T., Joanna Wysocka et Winship Herr. « Inactivation of the Retinoblastoma Protein Family Can Bypass the HCF-1 Defect in tsBN67 Cell Proliferation and Cytokinesis ». Molecular and Cellular Biology 22, no 19 (1 octobre 2002) : 6767–78. http://dx.doi.org/10.1128/mcb.22.19.6767-6778.2002.
Texte intégralScoggin, Kirsten E. S., Aida Ulloa et Jennifer K. Nyborg. « The Oncoprotein Tax Binds the SRC-1-Interacting Domain of CBP/p300 To Mediate Transcriptional Activation ». Molecular and Cellular Biology 21, no 16 (15 août 2001) : 5520–30. http://dx.doi.org/10.1128/mcb.21.16.5520-5530.2001.
Texte intégralThèses sur le sujet "Oncoproteina Tax"
AVESANI, Francesca. « Studio delle interazioni della oncoproteina Tax dei retrovirus HTLV con i fattori cellulari della via NF-kB ». Doctoral thesis, Università degli Studi di Verona, 2009. http://hdl.handle.net/11562/337341.
Texte intégralHuman T-cell lymphotropic viruses type 1 and type 2 (HTLV-1 and HTLV-2) are related oncoviruses that have been associated with lymphoproliferative and neurodegenerative disorders. The transactivator Tax protein, encoded by the pX region of HTLV genome, is a key factor in cellular transformation. HTLV-1 Tax oncoprotein (Tax-1) reprograms G1 to S progression through multiple mechanistic ways as well as protein-protein binding, transcriptional induction/repression, and post-translational modifications. HTVL-2 Tax (Tax-2) shares more than 70% aa homology whit Tax-1, however Tax-2 has a lower transforming activity than Tax-1. Based on this difference the structural and functional study of Tax proteins can be useful to understand the cellular mechanisms that more specifically take part in oncogenesis. Tax-1 is a 40 KDa transactivator protein which regulates viral transcription by modulating the activity of cellular factors involved in several signal transduction pathways. Tax-1 activation of NF-kB signalling is critical for cellular transformation and while its interaction with NF-kB factors have been intensively investigated little is known about Tax-2 interaction with cellular proteins of this pathway. The aim of this research is the comparison of Tax-2 and Tax-1 for the ability to activate NF-kB pathway. We studied Tax-2 interactions with factors of NF-kB signalling and the contribution of Tax-1 post-translational modifications in the protein-protein interaction. We chose three factors involved in the canonical NF- kB cascade: the transcription factor p65/RelA, the upstream signaling activator TAB2, and the IKKe kinase. In this research, we provide, for the first time, evidence of the involvement of the transcription factor p65/RelA and the protein TAB2 (TAK1 binding protein 1) in Tax-2B-mediated NF-kB activation. In fact, we demonstrate the association of Tax-2B with p65/RelA and TAB2 in co-immunoprecipitation assays in human cells and, by luciferase assays, we highlight the cooperative effect of p65 and/or TAB2 on Tax-2-mediated gene expression activation from NF-kB promoter. Tax- 2/p65 recognition was also shown by in vitro GST-pull-down assays. We also demonstrate that TAB2 is interacting with Tax-2B through a domain that is necessary to form a complex that activates NF-kB cascade. Further analysis of Tax interaction with cellular factors involved in the NF-kB signaling, using the same methodology, identifies a novel interaction between Tax-1 and Tax-2 and IKKe factor, a kinase that mediates inducible phosphorylation of p65/RelA and IkBa. Considering the contribution of Tax-1 post-translational modifications in NF-kB induction and in association with cellular factors, we tested the ability of specific Tax-1 mutants to recognize p65, TAB2 and IKKe by co-immunoprecipitation experiments. The results of this analysis exclude a role of Tax-1 post-translational modifications in the association with these factors. In conclusion, the results obtained in the present study, suggest that Tax-1 and Tax-2B share similar, though not identical, abilities to associate and activate factors of canonical NF-kB pathway. Although we cannot at present explain this diversity, it is tempting to speculate that the differences of the two viral proteins in deregulating signal transduction pathways might be partially attributed to their different capacities to interact with non-canonical NF-kB pathway factors. Comparative studies of Tax-1 and Tax-2 association with cellular factors specifically involved in alternative NF-kB signaling will give new insight to clarify this hypothesis.
Walsh, Claire. « Human T-cell leukaemia virus type 1 tax oncoprotein identification of novel celluar interaction partners ». Thesis, University of Manchester, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.499848.
Texte intégralMann, Melanie Verfasser], et Bernhard [Akademischer Betreuer] [Fleckenstein. « The interplay between the viral oncoprotein Tax and the transcription elongation factor ELL2 / Melanie Mann. Gutachter : Bernhard Fleckenstein ». Erlangen : Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), 2015. http://d-nb.info/1075835720/34.
Texte intégralKelly, Gloria Domingo. « Repression of Tat-transactived HIV-LTR directed gene expression by E1A 12S oncoprotein ». Thesis, Georgia Institute of Technology, 1994. http://hdl.handle.net/1853/25227.
Texte intégralTollenaere, Armelle. « Étude de la balance transcriptionnelle du rétrovirus HTLV-1 : identification d'un nouveau mécanisme de répression de la transcription antisens du rétrovirus HTLV-1 par la transcription sens Hijacking of the O-GlcNAcZYME complex by the HTLV-1 Tax oncoprotein facilitates viral transcription ». Thesis, Sorbonne Paris Cité, 2019. https://wo.app.u-paris.fr/cgi-bin/WebObjects/TheseWeb.woa/wa/show?t=2091&f=16975.
Texte intégralHTLV-1 retrovirus infects mainly T CD4 lymphocytes and is the causative agent of Adult T cell Leukemia and an inflammatory pathology targeting the central nervous system named Tropical spastic paraparesis. The oncogenic properties of this virus lay in the expression of two oncoproteins, Tax and HBZ. Tax and all viral products except for HBZ are produced from the sense promoter of the virus located in the 5'LTR (Long Terminal Repeat). HTLV-1 antisense transcription leads to the synthesis of two transcripts one spliced, sHBZ, the other one unspliced, usHBZ. These two RNAs once translated give birth to two HBZ protein in which only a few amino acid differ in N-terminal extremity of the proteins. Tax and HBZ induce T lymphocytes proliferation, genomic abnormalities, lymphocytes immortalisation, ... Yet in leukemic cells, most of the time, Tax expression is lost, often by epigenetic repression of the 5'LTR. Thus even if Tax and HBZ actively take part in leukemic clones emergence, HTLV-1 transcriptional balance is deregulated in favor of HBZ at the final stage of transformation. In order to better comprehend how HTLV-1 leads to the development of leukemia, it is essential to understand how HTLV-1 transcriptional balance is regulated in the first steps of HTLV-1 infection. Whereas HBZ inhibitory effect on sense transcription is well described, little is known on the effect of sense transcription on HBZ expression. In this study, it has been shown that sHBZ promoter is less active in HTLV-1 infected lymphocytes with an active sense transcription. To confirm this observation, two pharmacological inhibitors of sense transcription have been caracterized and used to analyze the effect of a change in sense transcription level on sHBZ and usHBZ production. The inhibition of sense transcription is shown to inhibit usHBZ expression and enhance sHBZ transcription. The two antisense transcripts thus exhibit opposite patterns regarding sense transcription. To better define how this repression on sHBZ production is established and how the two promoters in the 3'LTR are regulated, a new model has been built. Jurkat T cells are stably transfected with a plasmid allowing the expression of sense transcripts under the control of the CMV promoter or a plasmid without sense transcription. These models will allow a precise characterization of sHBZ and usHBZ promoter and the deciphering of the inhibition initiated by sense transcription on sHBZ expression
TURCI, Marco. « Studio dell'espressione in cellule umane dell'oncoproteina Tax dei virus leucemogeni umani HTLV-1 e HTLV-2 ». Doctoral thesis, 2008. http://hdl.handle.net/11562/337631.
Texte intégralThe research activity carried out in this thesis covered two different projects. The first one concerns the problem of the infection by the retrovirus HTLV-2 of Italian intravenous drug users who are also infected by HIV-1, to understand the interaction between the two retroviruses at the cellular level and define the effect of coinfection on AIDS progression. The second is centered on the study and function of Tax proteins of HTLV-1 (Tax-1) and HTLV-2 (Tax-2) and the characterization by mutagenesis of specific protein domains that modulate their function. The first project entailed the development of quantitative PCR analysis and the determination of the proviral load of HTLV-2 in infected subjects and the molecular characterization of HTLV-2 isolates. From the analyses carried out on these subjects it was found that the number of long term non-progressors for AIDS is significantly higher among HIV-1/HTLV-2 coinfected patients than HIV-1 monoinfected cases. These data clearly indicate that HTLV-2 is exerting a protective effect against AIDS progression. Five coinfected subjects undergoing antiretroviral therapy showed a significant increase in HTLV-2 proviral load concomitant to a decrease in HIV-1 viremia, suggesting that the treatment against HIV-1 is ineffective against HTLV-2 infection. The first part of the second project involved the analysis of Tax-2 localization. To this end, tax-2 gene was cloned into an expression vector adding in frame the Green Fluorescent Protein (GFP) to C-term end. The transient expression in HeLa and 293T cells and the detection by fluorescent microscopy revealed that Tax-2 was preferentially distributed in the cytoplasm and formed single dots. To possibly understand the role of C-terminal domain in protein localization, the same expression procedure was performed for Tax-2 mutants progressively truncated at the C-term and merged with GFP: 331-GFP, GFP 156-, 115-GFP, 60-GFP. Fluorescence microscopy confirmed that Tax-2 was localized in the cytoplasm, with the exception of mutant 60-GFP, which was exclusively nuclear. Further reduction to 33 aa fragment showed a widespread cellular fluorescence, similarly that obtained for full length Tax-2-GFP. These data confirmed the presence of a "nuclear localization determinant" (NLD) in the first 60 aa of Tax-2. To more precisely characterize this N-terminal part of the protein, several mutants for single or small amino acid deletions of clone 60- GFP were analyzed. All clones, with the exception of a mutant with 17-20 deletion, presented a nuclear localization, indicating that point mutations are not changing NLD function. Instead, by removing the first 21 aa, NLD function was lost, suggesting that the first 41 aa are necessary for NLD function. The second part of the project on Tax function was centered on the study of comparative cellular localization of Tax-1 and Tax-2. Tax-1 and tax-2 were cloned by adding in frame at C-term different types of protein tags: GFP, Yellow Fluorescent Protein (YFP) (~ 27 KDa ), Halo protein (~ 30 KDa) and a sequence of 32 amino acid containing the epitope V5 (~ 3 KDa). The expression of Tax-1, -GFP, -YFP, -Halo and -V5 showed a predominantly nuclear localization, whereas that of Tax-2 linked to GFP, YFP or Halo was predominantly cytoplasmic. When Tax-2 was cloned and expressed using the small tag V5, a predominantly nuclear localization was obtained. These results demonstrated that using tags of different sizes can induce different localizations of the two proteins. To identify the regions of the two proteins involved in regulating cellular localization, Tax-1 and Tax-2 mutants progressively truncated at the C-term and merged with the tag V5 were constructed and expressed. A very similar cellular distribution for Tax-1 and Tax-2 was obtained, as visualized by confocal microscopy: predominantly nuclear for both Tax-1 and Tax-2 full length and 1- 340 forms and cytoplasmic for truncated mutants below the first 300 aa. Since no adequate antibody is available to recognise native Tax-2 expression inside the cell, adding a tag to the terminal parts of the protein becomes necessary, though these conformational changes could result in abnormal localization effect. It was thus decided to prepare constructs for Tax -1 and Tax-2 expression by inserting internally to the protein structure the tag Flag- H6 between amino acids 337 and 338. By comparing the localization of native Tax-1 without tags and Tax-1 with the 337 Flag-H6, it was found that this does not interfere with the mechanisms regulating Tax-1 localization and function. It was also found that 337 Flag-H6 presented a nuclear localization and was adequately functional. Using this expression system allowed to show that also Tax-2 is located in specific nuclear complexes that are similar, but not identical, to the nuclear bodies (NB) formed by Tax-1 and that their expression is responsible for a specific accumulation of RelA NFKB factor at nuclear level. In conclusion, this study has allowed further understanding of the crossinteraction between HTLV-2 and HIV in coinfected subjects, and has given new important clues on the problem of cellular distribution and function of Tax-1 and Tax-2. The complex mechanisms that are responsible for the pleiotropic activities of the two proteins will be further clarified in the future by investigating their post-translational modifications.
Thoma-Kreß, Andrea [Verfasser]. « The Tax protein of human T-cell lymphotropic virus type 1 (HTLV-1) as multifunctional oncoprotein = Das Tax-Protein des humanen T-Zell-lymphotropen Virus Typ 1 (HTLV-1) als multifunktionelles Onkoprotein / vorgelegt von Karin Andrea Kreß ». 2011. http://d-nb.info/1010536974/34.
Texte intégralChapitres de livres sur le sujet "Oncoproteina Tax"
Yoshida, M., T. Suzuki, J. Fujisawa et H. Hirai. « HTLV-1 Oncoprotein Tax and Cellular transcription Factors ». Dans Transacting Functions of Human Retroviruses, 79–89. Berlin, Heidelberg : Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-78929-8_4.
Texte intégralKfoury, Youmna, Rihab Nasr, Chloé Journo, Renaud Mahieux, Claudine Pique et Ali Bazarbachi. « The Multifaceted Oncoprotein Tax ». Dans Advances in Cancer Research, 85–120. Elsevier, 2012. http://dx.doi.org/10.1016/b978-0-12-394280-7.00003-8.
Texte intégralLow, Kenneth G., et Kuan-Teh Jeang. « Human t-cell leukemia virus type i oncoprotein, tax : Cell cycle dysregulation and cellular transformation ». Dans Perspectives in Medical Virology, 309–19. Elsevier, 2001. http://dx.doi.org/10.1016/s0168-7069(01)05011-x.
Texte intégralActes de conférences sur le sujet "Oncoproteina Tax"
Shatat, M. A., E. Yuan et R. T. Lee. « Mistletoe Lectin as Treatment for Small Cell Lung Cancer Expressing Myc Family Oncoproteins ». Dans American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a3950.
Texte intégralForlani, Greta, Rawan Abdallah, Roberto S. Accolla et Giovanna Tosi. « Abstract B048 : The MHC class II transactivator CIITA inhibits the persistent activation of NF-kB by Human T cell Lymphotropic Virus type-1 Tax-1 oncoprotein ». Dans Abstracts : CRI-CIMT-EATI-AACR Inaugural International Cancer Immunotherapy Conference : Translating Science into Survival ; September 16-19, 2015 ; New York, NY. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/2326-6074.cricimteatiaacr15-b048.
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