Polθ is phosphorylated by PLK1 to repair double-strand breaks in mitosis
暂无分享,去创建一个
S. Zinn-Justin | D. Loew | F. Dingli | J. Guirouilh-Barbat | E. Del Nery | Raphael Ceccaldi | R. Ghouil | C. Gelot | Rania Ghouil | Marton Tibor Kovacs | Simona Miron | Emilie Mylne | Alexis Haan | Liza Boeffard-Dosierre | Tatiana Popova | Elaine Del Nery | Sophie Zinn-Justin | Florent Dingli
[1] A. Triller,et al. Microglial TNFα orchestrates protein phosphorylation in the cortex during the sleep period and controls homeostatic sleep , 2022, The EMBO journal.
[2] A. Heijink,et al. Sister chromatid exchanges induced by perturbed replication can form independently of BRCA1, BRCA2 and RAD51 , 2022, Nature Communications.
[3] Toshiro K. Ohsumi,et al. The CIP2A–TOPBP1 axis safeguards chromosome stability and is a synthetic lethal target for BRCA-mutated cancer , 2021, Nature Cancer.
[4] M. Löbrich,et al. POLθ-mediated end joining is restricted by RAD52 and BRCA2 until the onset of mitosis , 2021, Nature Cell Biology.
[5] Oriol Vinyals,et al. Highly accurate protein structure prediction with AlphaFold , 2021, Nature.
[6] D. Fox,et al. Persistent DNA damage signaling and DNA polymerase theta promote broken chromosome segregation , 2021, bioRxiv.
[7] A. Tutt,et al. Polθ inhibitors elicit BRCA-gene synthetic lethality and target PARP inhibitor resistance , 2021, Nature Communications.
[8] J. Tainer,et al. A first-in-class Polymerase Theta Inhibitor selectively targets Homologous-Recombination-Deficient Tumors , 2021, Nature Cancer.
[9] J. Sekelsky,et al. DNA polymerase theta suppresses mitotic crossing over , 2020, bioRxiv.
[10] J. Sekelsky,et al. Mechanistic basis for microhomology identification and genome scarring by polymerase theta , 2019, Proceedings of the National Academy of Sciences.
[11] J. D. den Dunnen,et al. Templated Insertions: A Smoking Gun for Polymerase Theta-Mediated End Joining. , 2019, Trends in genetics : TIG.
[12] N. Willis,et al. DNA double-strand break repair-pathway choice in somatic mammalian cells , 2019, Nature Reviews Molecular Cell Biology.
[13] L. Pearl,et al. MDC1 Interacts with TOPBP1 to Maintain Chromosomal Stability during Mitosis , 2019, Molecular cell.
[14] D. Pellman,et al. Mitotic CDK Promotes Replisome Disassembly, Fork Breakage, and Complex DNA Rearrangements. , 2019, Molecular cell.
[15] Julian Spies,et al. 53BP1 nuclear bodies enforce replication timing at under-replicated DNA to limit heritable DNA damage , 2019, Nature Cell Biology.
[16] Martin Eisenacher,et al. The PRIDE database and related tools and resources in 2019: improving support for quantification data , 2018, Nucleic Acids Res..
[17] M. Jasin,et al. BRCA2 suppresses replication stress-induced mitotic and G1 abnormalities through homologous recombination , 2017, Nature Communications.
[18] R. Pomerantz,et al. The helicase domain of Polθ counteracts RPA to promote alt-NHEJ , 2017, Nature Structural & Molecular Biology.
[19] Alan Ashworth,et al. PARP inhibitors: Synthetic lethality in the clinic , 2017, Science.
[20] Daniel Durocher,et al. The control of DNA repair by the cell cycle , 2016, Nature Cell Biology.
[21] David W. Wyatt,et al. Essential Roles for Polymerase θ-Mediated End Joining in the Repair of Chromosome Breaks. , 2016, Molecular cell.
[22] A. D’Andrea,et al. FANCD2 Maintains Fork Stability in BRCA1/2-Deficient Tumors and Promotes Alternative End-Joining DNA Repair. , 2016, Cell reports.
[23] Y. Liu,et al. Replication stress activates DNA repair synthesis in mitosis , 2015, Nature.
[24] Kyle M. Miller,et al. Mammalian polymerase θ promotes alternative NHEJ and suppresses recombination , 2015, Nature.
[25] Stephen J. Elledge,et al. Homologous recombination-deficient tumors are hyper-dependent on POLQ-mediated repair , 2015, Nature.
[26] R. Pomerantz,et al. Mechanism of Microhomology-Mediated End-Joining Promoted by Human DNA Polymerase Theta , 2014, Nature Structural &Molecular Biology.
[27] David W. Wyatt,et al. Mechanism of Suppression of Chromosomal Instability by DNA Polymerase POLQ , 2014, PLoS genetics.
[28] A. Carr,et al. TopBP1: A BRCT-scaffold protein functioning in multiple cellular pathways. , 2014, DNA repair.
[29] A. Shinohara,et al. Canonical Non-Homologous End Joining in Mitosis Induces Genome Instability and Is Suppressed by M-phase-Specific Phosphorylation of XRCC4 , 2014, PLoS genetics.
[30] G. Adelmant,et al. Dephosphorylation enables the recruitment of 53BP1 to double-strand DNA breaks. , 2014, Molecular cell.
[31] D. Durocher,et al. Mitosis Inhibits DNA Double-Strand Break Repair to Guard Against Telomere Fusions , 2014, Science.
[32] M. Tijsterman,et al. Polymerase theta-mediated end joining of replication-associated DNA breaks in C. elegans , 2014, Genome research.
[33] Wouter Koole,et al. A Polymerase Theta-dependent repair pathway suppresses extensive genomic instability at endogenous G4 DNA sites , 2014, Nature Communications.
[34] K. Cimprich,et al. Causes and consequences of replication stress , 2013, Nature Cell Biology.
[35] A. Heijink,et al. The DNA damage response during mitosis. , 2013, Mutation research.
[36] J. Glover,et al. Structural insights into recognition of MDC1 by TopBP1 in DNA replication checkpoint control. , 2013, Structure.
[37] Johannes E. Schindelin,et al. Fiji: an open-source platform for biological-image analysis , 2012, Nature Methods.
[38] S. Knapp,et al. Rapid determination of multiple linear kinase substrate motifs by mass spectrometry. , 2012, Chemistry & biology.
[39] B. Chait,et al. Cdk1 uncouples CtIP-dependent resection and Rad51 filament formation during M-phase double-strand break repair , 2011, The Journal of cell biology.
[40] Otto Hudecz,et al. Spatial Exclusivity Combined with Positive and Negative Selection of Phosphorylation Motifs Is the Basis for Context-Dependent Mitotic Signaling , 2011, Science Signaling.
[41] B. Neumann,et al. 53BP1 nuclear bodies form around DNA lesions generated by mitotic transmission of chromosomes under replication stress , 2011, Nature Cell Biology.
[42] S. Jackson,et al. DNA damage signaling in response to double-strand breaks during mitosis , 2010, The Journal of cell biology.
[43] M. McVey,et al. Dual Roles for DNA Polymerase Theta in Alternative End-Joining Repair of Double-Strand Breaks in Drosophila , 2010, PLoS genetics.
[44] M. McVey,et al. Synthesis-dependent microhomology-mediated end joining accounts for multiple types of repair junctions , 2010, Nucleic acids research.
[45] Aideen Long,et al. Statistical methods for analysis of high-throughput RNA interference screens , 2009, Nature Methods.
[46] P. Jeggo,et al. Chromosome breakage after G2 checkpoint release , 2007, The Journal of cell biology.
[47] Wayne Boucher,et al. The CCPN data model for NMR spectroscopy: Development of a software pipeline , 2005, Proteins.
[48] S. West,et al. CDK-dependent phosphorylation of BRCA2 as a regulatory mechanism for recombinational repair , 2005, Nature.
[49] P. Jallepalli,et al. Chromosome segregation and cancer: cutting through the mystery , 2001, Nature Reviews Cancer.
[50] R. Espinosa,et al. Replication of a common fragile site, FRA3B, occurs late in S phase and is delayed further upon induction: implications for the mechanism of fragile site induction. , 1998, Human molecular genetics.
[51] F. M. Davis,et al. Monoclonal antibodies to mitotic cells. , 1983, Proceedings of the National Academy of Sciences of the United States of America.
[52] A. D’Andrea,et al. Repair Pathway Choices and Consequences at the Double-Strand Break. , 2016, Trends in cell biology.
[53] R. Wood,et al. DNA polymerase POLQ and cellular defense against DNA damage. , 2013, DNA repair.