Literatura científica selecionada sobre o tema "Paralogues de Rad51"
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Artigos de revistas sobre o assunto "Paralogues de Rad51"
Tarsounas, Madalena, Adelina A. Davies e Stephen C. West. "RAD51 localization and activation following DNA damage". Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 359, n.º 1441 (29 de janeiro de 2004): 87–93. http://dx.doi.org/10.1098/rstb.2003.1368.
Texto completo da fonteGodin, Stephen K., Meghan R. Sullivan e Kara A. Bernstein. "Novel insights into RAD51 activity and regulation during homologous recombination and DNA replication". Biochemistry and Cell Biology 94, n.º 5 (outubro de 2016): 407–18. http://dx.doi.org/10.1139/bcb-2016-0012.
Texto completo da fonteLiu, Jie, Ludovic Renault, Xavier Veaute, Francis Fabre, Henning Stahlberg e Wolf-Dietrich Heyer. "Rad51 paralogues Rad55–Rad57 balance the antirecombinase Srs2 in Rad51 filament formation". Nature 479, n.º 7372 (23 de outubro de 2011): 245–48. http://dx.doi.org/10.1038/nature10522.
Texto completo da fonteAngelis, Karel J., Lenka Záveská Drábková, Radka Vágnerová e Marcela Holá. "RAD51 and RAD51B Play Diverse Roles in the Repair of DNA Double Strand Breaks in Physcomitrium patens". Genes 14, n.º 2 (24 de janeiro de 2023): 305. http://dx.doi.org/10.3390/genes14020305.
Texto completo da fonteKhoo, Kelvin H. P., Hayley R. Jolly e Jason A. Able. "The RAD51 gene family in bread wheat is highly conserved across eukaryotes, with RAD51A upregulated during early meiosis". Functional Plant Biology 35, n.º 12 (2008): 1267. http://dx.doi.org/10.1071/fp08203.
Texto completo da fontePohl, Thomas J., e Jac A. Nickoloff. "Rad51-Independent Interchromosomal Double-Strand Break Repair by Gene Conversion Requires Rad52 but Not Rad55, Rad57, or Dmc1". Molecular and Cellular Biology 28, n.º 3 (26 de novembro de 2007): 897–906. http://dx.doi.org/10.1128/mcb.00524-07.
Texto completo da fonteGodin, Stephen, Adam Wier, Faiz Kabbinavar, Dominique S. Bratton-Palmer, Harshad Ghodke, Bennett Van Houten, Andrew P. VanDemark e Kara A. Bernstein. "The Shu complex interacts with Rad51 through the Rad51 paralogues Rad55–Rad57 to mediate error-free recombination". Nucleic Acids Research 41, n.º 8 (4 de março de 2013): 4525–34. http://dx.doi.org/10.1093/nar/gkt138.
Texto completo da fonteBadie, Sophie, Chunyan Liao, Maria Thanasoula, Paul Barber, Mark A. Hill e Madalena Tarsounas. "RAD51C facilitates checkpoint signaling by promoting CHK2 phosphorylation". Journal of Cell Biology 185, n.º 4 (18 de maio de 2009): 587–600. http://dx.doi.org/10.1083/jcb.200811079.
Texto completo da fonteYang, Yongjia, Jihong Guo, Lei Dai, Yimin Zhu, Hao Hu, Lihong Tan, Weijian Chen et al. "XRCC2 mutation causes meiotic arrest, azoospermia and infertility". Journal of Medical Genetics 55, n.º 9 (24 de julho de 2018): 628–36. http://dx.doi.org/10.1136/jmedgenet-2017-105145.
Texto completo da fonteRoy, Upasana, e Eric C. Greene. "The Role of the Rad55–Rad57 Complex in DNA Repair". Genes 12, n.º 9 (8 de setembro de 2021): 1390. http://dx.doi.org/10.3390/genes12091390.
Texto completo da fonteTeses / dissertações sobre o assunto "Paralogues de Rad51"
Dupont, Chloé. "Régulation de la formation des nucléofilaments Rad51 par les complexes de paralogues de Rad51 chez la levure Saccharomyces cerevisiae". Electronic Thesis or Diss., université Paris-Saclay, 2024. http://www.theses.fr/2024UPASL009.
Texto completo da fonteHomologous recombination (HR) is one of the major repair pathways for DNA damage such as double-strand breaks (DSBs). This pathway is also involved in restarting replication forks stalled by DNA lesion. A key step in this repair pathway involves the formation of nucleoprotein filaments formed by Rad51 recombinase on single-stranded DNA (ssDNA). These nucleofilaments are responsible for homology search and invasion of an intact DNA similar to the damaged DNA in order to use it as a template for repair synthesis. The formation of these nucleofilaments is tightly regulated. In the budding yeast Saccharomyces cerevisiae, the formation of Rad51 filaments is ensured by positive regulators such as the Rad52 mediator protein and the two complexes composed of Rad51 paralogue proteins, the Rad55-Rad57 complex and the SHU complex. They also play a role in protecting this nucleofilament from the negative regulator Srs2 by counterbalancing its disassembly effects. To gain a better understanding of the regulatory mechanism of the Rad51 nucleofilament, we need a more detailed understanding of the complex interactions between these multiple players. During my thesis, we aimed at determining the structure of Rad51 paralog complexes in association with Rad51 filaments. To do this, we combined a structural bioinformatics approach, based on sequence alignments and the published structure of Rad51, with yeast two-hybrid (Y2H) experiments. This strategy allowed us to build for the first time a model for the organisation of Rad51 paralog complexes, the Rad55-Rad57 and SHU complexes, in association with the Rad51 recombinase. This model was further validated by genetic analysis of mutations disrupting each interaction domain. In our model, Rad55-Rad57 adopts a similar structure than a dimer of Rad51 and it interacts only with the 5'-end of Rad51 filaments and only through the Rad57 subunit. Our genetic analyses suggest that the major role of the interaction between Rad55-Rad57 and Rad51 is to protect Rad51 filaments against the Srs2 translocase. On the other side of Rad55-Rad57, Rad55 interacts with the Csm2 subunit of the SHU complex through its N-terminal end. Interestingly, our genetic analyses revealed that SHU and the N-terminal end of Rad55 are dispensable for DSB repair. However, they are involved in the repair of UV-induced single-strand breaks. We propose that the SHU complex stabilizes the binding of Rad55-Rad57 on ssDNA gaps, thereby promoting enhanced stability of Rad51 filaments. Thus, Rad51 filaments would be more resistant to the destabilising activity of the Srs2 translocase and would allow HR to compete with alternative gap filling pathways involving error-prone translesion DNA polymerases. Our data allow us to propose a model for the installation of the Rad51 filament by paralog complexes, Rad55-Rad57 and SHU, in collaboration with Rad52
Dobson, Rachel Pamela. "Analysis of the functions and interactions of RAD51 paralogues in Trypanosoma brucei". Thesis, University of Glasgow, 2009. http://theses.gla.ac.uk/939/.
Texto completo da fonteRodrigue, Amélie. "Rôles des paralogues de RAD51 humains dans la recombinaison homologue et le maintien de la stabilité du génome en mitose". Thesis, Université Laval, 2011. http://www.theses.ulaval.ca/2011/27916/27916.pdf.
Texto completo da fonteDaboussi, Fayza. "Relations épistatiques entre RAD51 et ses paralogues chez les mammifères : étude de la sensibilité aux stress génotoxiques, la recombinaison homologue, la duplication des centrosomes et la réplication". Paris 7, 2005. http://www.theses.fr/2005PA077199.
Texto completo da fonteHomologous recombination (HR) is a fundamental biological process, conserved in all organisms. In mammals, Rad51 protein and its paralogues are involved in this process. Here, we address the question whether RAD51 and its paralogs act in the same pathway. To answer this question, we examined the consequences of the overexpression of a dominant negative form of RAD51 in the irs 1 cell line, mutated in the XRCC2 paralogue gene. This work demonstrated that Rad51 and Xrcc2 proteins act in the same. . Pathway with respect to résistance to genotoxic stresses, homologous recombination and centrosome duplication. In cell lines defective for HR, we also observed a slowing down in the progression of replication forks and the activation of S/G2 checkpoint dependent on ATM/ATR
Oliveira, Ana Clara. "Influência do gene PTEN na expressão de RAD51 e suas parálogas, RAD51C e RAD51B, em linhagens de glioblastoma multiforme tratadas com etoposídeo". Universidade de São Paulo, 2016. http://www.teses.usp.br/teses/disponiveis/17/17135/tde-27072016-143803/.
Texto completo da fonteGlioblastoma multiforme (GBM) is the most common malignant brain tumor. Loss of PTEN (Phosphatase and tensin homolog deleted on chromosome 10) gene is the most frequent alteration associated with GBM and encodes a phosphatase enzyme that antagonizes the PI3K, by inhibiting AKT phosphorylation thereby regulating signaling pathways related to cell survival and proliferation. PTEN deficiency has been associated with genomic instability and increased endogenous DSBs, as well as reduced expression of RAD51, which is a key gene with crucial role in HR. In this study, we aimed to evaluate whether the PTEN status in GBM cell lines can affect RAD51 expression and HR efficiency under conditions of treatment with the antineoplastic drug etoposide, which targets the DNA topoisomerase II enzyme, thus leading to the production of DNA breaks. T98G (PTEN mutated) and LN18 (PTEN wild-type) cells were treated with etoposide, and several assays were carried out: cell proliferation, detection and quantification of necrosis and apoptosis, cell cycle kinetics, immunofluorescence staining, RAD51 (and paralogs) protein expression, and PTEN silencing in LN18 cell line, by using the siRNA method. LN18 cells showed a greater reduction in cell proliferation, compared to T98G after treatments (25, 50, 75 e 100 µM) at 24, 72 and 120h. Both cell lines showed a significant increase (p=<0.001) in cell death induction, but LN18 presented a greater percentage of apoptotic and necrotic cells than T98G (24, 72 and 120h). The induction of DSB was analyzed by immunostaining (with ?-H2AX antibody), and for the concentrations (50 and 75 µM) tested, LN18 showed higher levels of ?-H2AX positive cells than that observed for T98G (p=<0.001). The analysis of cell cycle kinetics performed for cells treated with etoposide (50 and 75 µM) and collected at 24, 48 and 72h, LN18 presented a greater G2-blockage, as compared to T98G; only LN18 showed a blockage at the S-phase. The expression of RAD51, RAD51B and C was higher in LN18 compared to T98G and U87MG cells treated with etoposide (75 µM) and controls. When we silenced PTEN in LN18 linage, to check if PTEN silencing may reduce the expression of RAD51 and its paralogs, we found a 69.9% reduction in PTEN protein expressions, and the expression of RAD51 and RAD51C was also found reduced, compared to the control group. Taken together, the results obtained in this study indicate that the status of PTEN is critical for survival pathways, cell cycle control and induction of apoptosis in GBM cells, confirming the relationship between PTEN and RAD51 and its paralogs in GBM cells treated with an inducer of DNA breaks. These results contribute with relevant information for further studies on molecular pathways underlying the interaction between PTEN and RAD51 and its paralogs
Taylor, M. R. G. "Mechanism of action of Rad51 paralogs". Thesis, University College London (University of London), 2015. http://discovery.ucl.ac.uk/1458671/.
Texto completo da fonteVan, Laar Tricia A. "The behavior of RAD51D and XRCC2 in response to drug induced DNA damage and a continuing study of the fly RAD51 paralogs". Scholarly Commons, 2011. https://scholarlycommons.pacific.edu/uop_etds/764.
Texto completo da fonteHaldenby, Sam. "Genetic analysis of RadB, a paralogue of the archaeal Rad51/RecA homologue, RadA". Thesis, University of Nottingham, 2007. http://eprints.nottingham.ac.uk/10384/.
Texto completo da fonteAmunugama, Ravindra Bandara. "Insights into Regulation of Human RAD51 Nucleoprotein Filament Activity During Homologous Recombination". The Ohio State University, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=osu1321984760.
Texto completo da fonteSaini, Siddharth. "Role of XRCC3 in Acquisition and Maintenance of Invasiveness through Extracellular Matrix in Breast Cancer Progression". VCU Scholars Compass, 2010. http://scholarscompass.vcu.edu/etd/131.
Texto completo da fonteCapítulos de livros sobre o assunto "Paralogues de Rad51"
Roy, Upasana, Youngho Kwon, Patrick Sung e Eric C. Greene. "Single-molecule studies of yeast Rad51 paralogs". In Methods in Enzymology, 343–62. Elsevier, 2021. http://dx.doi.org/10.1016/bs.mie.2021.08.006.
Texto completo da fonte