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Artykuły w czasopismach na temat "Ligase IV/XRCC4"
Nick McElhinny, Stephanie A., Carey M. Snowden, Joseph McCarville i Dale A. Ramsden. "Ku Recruits the XRCC4-Ligase IV Complex to DNA Ends". Molecular and Cellular Biology 20, nr 9 (1.05.2000): 2996–3003. http://dx.doi.org/10.1128/mcb.20.9.2996-3003.2000.
Pełny tekst źródłaWu, Peï-Yu, Philippe Frit, SriLakshmi Meesala, Stéphanie Dauvillier, Mauro Modesti, Sara N. Andres, Ying Huang i in. "Structural and Functional Interaction between the Human DNA Repair Proteins DNA Ligase IV and XRCC4". Molecular and Cellular Biology 29, nr 11 (30.03.2009): 3163–72. http://dx.doi.org/10.1128/mcb.01895-08.
Pełny tekst źródłaMalashetty, Vidyasagar, Audrey Au, Jose Chavez, Mary Hanna, Jennifer Chu, Jesse Penna i Patricia Cortes. "The DNA binding domain and the C-terminal region of DNA Ligase IV specify its role in V(D)J recombination". PLOS ONE 18, nr 2 (24.02.2023): e0282236. http://dx.doi.org/10.1371/journal.pone.0282236.
Pełny tekst źródłaMahajan, Kiran N., Stephanie A. Nick McElhinny, Beverly S. Mitchell i Dale A. Ramsden. "Association of DNA Polymerase μ (pol μ) with Ku and Ligase IV: Role for pol μ in End-Joining Double-Strand Break Repair". Molecular and Cellular Biology 22, nr 14 (15.07.2002): 5194–202. http://dx.doi.org/10.1128/mcb.22.14.5194-5202.2002.
Pełny tekst źródłaPrzewloka, Marcin R., Paige E. Pardington, Steven M. Yannone, David J. Chen i Robert B. Cary. "In Vitro and In Vivo Interactions of DNA Ligase IV with a Subunit of the Condensin Complex". Molecular Biology of the Cell 14, nr 2 (luty 2003): 685–97. http://dx.doi.org/10.1091/mbc.e01-11-0117.
Pełny tekst źródłaFrancis, Dailia B., Mikhail Kozlov, Jose Chavez, Jennifer Chu, Shruti Malu, Mary Hanna i Patricia Cortes. "DNA Ligase IV regulates XRCC4 nuclear localization". DNA Repair 21 (wrzesień 2014): 36–42. http://dx.doi.org/10.1016/j.dnarep.2014.05.010.
Pełny tekst źródłaRoy, Sunetra, Abinadabe J. de Melo, Yao Xu, Satish K. Tadi, Aurélie Négrel, Eric Hendrickson, Mauro Modesti i Katheryn Meek. "XRCC4/XLF Interaction Is Variably Required for DNA Repair and Is Not Required for Ligase IV Stimulation". Molecular and Cellular Biology 35, nr 17 (22.06.2015): 3017–28. http://dx.doi.org/10.1128/mcb.01503-14.
Pełny tekst źródłaRecuero-Checa, María A., Andrew S. Doré, Ernesto Arias-Palomo, Angel Rivera-Calzada, Sjors H. W. Scheres, Joseph D. Maman, Laurence H. Pearl i Oscar Llorca. "Electron microscopy of Xrcc4 and the DNA ligase IV–Xrcc4 DNA repair complex". DNA Repair 8, nr 12 (grudzień 2009): 1380–89. http://dx.doi.org/10.1016/j.dnarep.2009.09.007.
Pełny tekst źródłaHayden, Patrick, Prerna Tewari, Anthony Staines, Derek Morris, Dominique Crowley, Alexandra Nieters, Nicholas Becker i in. "Variation in DNA Repair Genes XRCC3, XRCC4, and XRCC5 and Risk of Myeloma." Blood 108, nr 11 (16.11.2006): 3416. http://dx.doi.org/10.1182/blood.v108.11.3416.3416.
Pełny tekst źródłaHsu, Hsin-Ling, Steven M. Yannone i David J. Chen. "Defining interactions between DNA-PK and ligase IV/XRCC4". DNA Repair 1, nr 3 (marzec 2002): 225–35. http://dx.doi.org/10.1016/s1568-7864(01)00018-0.
Pełny tekst źródłaRozprawy doktorskie na temat "Ligase IV/XRCC4"
Stiff, Thomas. "Characterisation of proteins that stimulate the DNA ligase IV/Xrcc4 complex". Thesis, University of Sussex, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.249402.
Pełny tekst źródłaWang, Yu. "Mismatch ligation during non-homologous end joining pathway kinetic characterization of human DNA ligase IV/XRCC4 complex /". Columbus, Ohio : Ohio State University, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1179947467.
Pełny tekst źródłaDe, Melo Abinadabe Jackson. "Molecular basis for the structural role of human DNA ligase IV". Thesis, Aix-Marseille, 2016. http://www.theses.fr/2016AIXM4040.
Pełny tekst źródłaFailure to repair DNA double-strand breaks (DSBs) may have deleterious consequences inducing genomic instability and even cell death. In most mammalian cells, Non-Homologous End Joining (NHEJ) is a prominent DSB repair pathway. DNA ligase IV (LigIV) is unique in its ability to promote classical NHEJ. It associates with two structurally related proteins called XRCC4 and XLF (aka Cernunnos). LigIV directly interacts with XRCC4 forming a stable complex while the XLF interaction with this complex is mediated by XRCC4. XLF strongly stimulates the ligation activity of the LigIV/XRCC4 complex by an unknown mechanism. Recently, a structural noncatalytic role of LigIV has been uncovered (Cottarel et al., 2013). Here, we have reconstituted the end joining ligation step using recombinant proteins produced in bacteria to explore not only the molecular basis for the structural role of LigIV, but also to understand the mechanism by which XLF stimulates the ligation complex, and how these three proteins work together during NHEJ. Our biochemical analysis suggests that XLF, through interactions with LigIV/XRCC4 complex, could induce a conformational change in LigIV. Rearrangement of the LigIV would expose its DNA binding interface that is able to bridge two independent DNA molecules. This bridging ability is fully independent of LigIV’s catalytic activity. We have mutated this interface in order to attempt to disrupt the newly identified DNA bridging ability. In vitro analysis of this LigIV mutant will be presented as well as a preliminary in vivo analysis
Ochi, Takashi. "Non-homologous end-joining DNA double strand break repair : structural studies of the DNA ligase IV/XRCC4 complex". Thesis, University of Cambridge, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609793.
Pełny tekst źródłaAmram, Jérémy. "Etude structurale et fonctionnelle des complexes multi-protéiques de la voie de réparation NHEJ chez l’homme". Thesis, Paris 11, 2015. http://www.theses.fr/2015PA114822/document.
Pełny tekst źródłaHuman DNA repair pathway NHEJ (Non-Homologous End-Joining) is a major pathway of double-strand breaks repair. The proteins involved in this pathway interact and form dynamic complexes whose molecular mechanisms are largely unknown. Firstly, we established protocols to be able to purify milligrams of those NHEJ pathway core proteins using MultiBac insect cells system. We then purified Ku70/Ku80 and Ligase4/XRCC4 complexes, Artemis and Cernunnos to homogeneity. Crystallogenesis assays, SAXS experiments and Transmission Electronic Microscopy experiments have been performed on several complexes formed by these core NHEJ proteins. We also characterized the interactions between these proteins by Size Exclusion Chromatography and Isothermal Calorimetry. These experiments have led to biochemical results sufficient to establish a solid basis to initiate the structural and functional study of the Human NHEJ Pathway
Menchon, Grégory. "Criblage virtuel et fonctionnel sur le complexe XRCC4/ADN ligase IV/Cer-XLF de ligature des cassures double-brin de l'ADN : application en radiosensibilisation tumorale". Thesis, Toulouse 3, 2015. http://www.theses.fr/2015TOU30395.
Pełny tekst źródłaRadiotherapy is a major weapon used against cancer. Radio-induced DNA double strand breaks (DSB) are the main lesions responsible for cell death. Non-homologous end-joining (NHEJ) is a predominant DSB repair mechanism which contributes to cancer cells resistance to radiotherapy. NHEJ is thus a good target for strategies which aim at increasing the radio-sensitivity of tumors. Through in silico screening and biophysical and biochemical assays, our objective was to find specific ligands for the XRCC4/Lig4 and XRCC4/Cer-XLF protein-protein interactions involved in NHEJ. Here, we isolated the first compounds able to prevent their interaction in vitro. These early stage inhibitors are promising tools for cancer therapy with the hope to develop more specific compounds for cellular assays through the 3D structure of the protein/inhibitor complexes
Tatavarthi, Haritha. "Action of Tyrosyl DNA Phosphodiesterase on 3'-Phosphoglycolate Terminated DNA Strand Breaks". VCU Scholars Compass, 2006. http://hdl.handle.net/10156/1799.
Pełny tekst źródłaPandey, Monica. "Understanding the Sequence Dependence of NHEJ Mediated Double-strand Break Repair, and Identification of Novel DNA Ligase Inhibitors and their Potential Use as Cancer Therapeutics". Thesis, 2017. http://etd.iisc.ac.in/handle/2005/4146.
Pełny tekst źródłaKsiążki na temat "Ligase IV/XRCC4"
Stiff, Thomas. Characterisation of proteins that stimulate the DNA Ligase IV/Xrcc4 complex. 2002.
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