Differences in the recruitment of DNA repair proteins at subtelomeric and interstitial I-SceI endonuclease-induced DNA double-strand breaks.

[1]  G. Iliakis,et al.  DNA double-strand-break repair in higher eukaryotes and its role in genomic instability and cancer: Cell cycle and proliferation-dependent regulation. , 2016, Seminars in cancer biology.

[2]  K. Rothkamm,et al.  Functional crosstalk between DNA damage response proteins 53BP1 and BRCA1 regulates double strand break repair choice. , 2016, Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology.

[3]  J. Murnane,et al.  Processing by MRE11 is involved in the sensitivity of subtelomeric regions to DNA double-strand breaks , 2015, Nucleic acids research.

[4]  M. Jasin,et al.  Homologous recombination and human health: the roles of BRCA1, BRCA2, and associated proteins. , 2015, Cold Spring Harbor perspectives in biology.

[5]  J. Jonkers,et al.  BRCA1 and CtIP promote alternative non‐homologous end‐joining at uncapped telomeres , 2015, The EMBO journal.

[6]  Zhihui Feng,et al.  53BP1 promotes microhomology-mediated end-joining in G1-phase cells , 2015, Nucleic acids research.

[7]  Jeremy M. Stark,et al.  DNA Damage Response Factors from Diverse Pathways, Including DNA Crosslink Repair, Mediate Alternative End Joining , 2015, PLoS genetics.

[8]  A. Tomkinson,et al.  Chromosomal translocations in human cells are generated by canonical nonhomologous end-joining. , 2014, Molecular cell.

[9]  J. Shiloach,et al.  CtIP maintains stability at common fragile sites and inverted repeats by end resection-independent endonuclease activity. , 2014, Molecular cell.

[10]  A. Shibata,et al.  DNA double-strand break repair in a cellular context. , 2014, Clinical oncology (Royal College of Radiologists (Great Britain)).

[11]  Michal Zimmermann,et al.  53BP1: pro choice in DNA repair. , 2014, Trends in cell biology.

[12]  Stéphanie Panier,et al.  Double-strand break repair: 53BP1 comes into focus , 2013, Nature Reviews Molecular Cell Biology.

[13]  Minli Wang,et al.  Investigation of switch from ATM to ATR signaling at the sites of DNA damage induced by low and high LET radiation. , 2013, DNA repair.

[14]  A. Porcellini,et al.  Targeted DNA methylation by homology-directed repair in mammalian cells. Transcription reshapes methylation on the repaired gene , 2013, Nucleic acids research.

[15]  A. Shibata,et al.  Opposing roles for 53BP1 during homologous recombination , 2013, Nucleic acids research.

[16]  M. Löbrich,et al.  ATM Release at Resected Double-Strand Breaks Provides Heterochromatin Reconstitution to Facilitate Homologous Recombination , 2013, PLoS genetics.

[17]  Linda Z. Shi,et al.  Microhomology-mediated End Joining and Homologous Recombination share the initial end resection step to repair DNA double-strand breaks in mammalian cells , 2013, Proceedings of the National Academy of Sciences.

[18]  S. Powell,et al.  Development of an assay to measure mutagenic non-homologous end-joining repair activity in mammalian cells , 2013, Nucleic acids research.

[19]  T. Ludwig,et al.  Double-strand break repair by homologous recombination in primary mouse somatic cells requires BRCA1 but not the ATM kinase , 2013, Proceedings of the National Academy of Sciences.

[20]  Adam P. Rosebrock,et al.  A cell cycle-dependent regulatory circuit composed of 53BP1-RIF1 and BRCA1-CtIP controls DNA repair pathway choice. , 2013, Molecular cell.

[21]  J. Murnane,et al.  The Role of ATM in the Deficiency in Nonhomologous End-Joining near Telomeres in a Human Cancer Cell Line , 2013, PLoS genetics.

[22]  B. Chait,et al.  Activation of DSB processing requires phosphorylation of CtIP by ATR. , 2013, Molecular cell.

[23]  J. Diedrich,et al.  A two-step mechanism for TRF2-mediated chromosome end protection , 2013, Nature.

[24]  J. Murnane,et al.  Mechanisms of telomere loss and their consequences for chromosome instability , 2012, Front. Oncol..

[25]  S. Boulton,et al.  Playing the end game: DNA double-strand break repair pathway choice. , 2012, Molecular cell.

[26]  Ran Kafri,et al.  Quantitative live cell imaging reveals a gradual shift between DNA repair mechanisms and a maximal use of HR in mid S phase. , 2012, Molecular cell.

[27]  Xiaolan Zhao,et al.  Homologous recombination and its regulation , 2012, Nucleic acids research.

[28]  F. D. D. Fagagna,et al.  Telomeric DNA damage is irreparable and causes persistent DNA-damage-response activation , 2012, Nature Cell Biology.

[29]  J. Murnane,et al.  Telomere dysfunction and chromosome instability. , 2012, Mutation research.

[30]  Clara Correia-Melo,et al.  Telomeres are favoured targets of a persistent DNA damage response in ageing and stress-induced senescence , 2012, Nature Communications.

[31]  E. Nam,et al.  ATR signalling: more than meeting at the fork. , 2011, The Biochemical journal.

[32]  M. Nussenzweig,et al.  Regulation of DNA end joining, resection, and immunoglobulin class switch recombination by 53BP1. , 2011, Molecular cell.

[33]  Jeremy M. Stark,et al.  Subtelomeric regions in mammalian cells are deficient in DNA double-strand break repair. , 2011, DNA repair.

[34]  S. Raghavan,et al.  How does DNA break during chromosomal translocations? , 2011, Nucleic acids research.

[35]  Stefano Ferrari,et al.  DNA end resection by CtIP and exonuclease 1 prevents genomic instability , 2010, EMBO reports.

[36]  Jeremy M. Stark,et al.  ATM Limits Incorrect End Utilization during Non-Homologous End Joining of Multiple Chromosome Breaks , 2010, PLoS genetics.

[37]  Jingsong Yuan,et al.  Focus on histone variant H2AX: To be or not to be , 2010, FEBS letters.

[38]  N. Manfrini,et al.  Mechanisms and regulation of DNA end resection , 2010, The EMBO journal.

[39]  M. Lieber,et al.  The mechanism of double-strand DNA break repair by the nonhomologous DNA end-joining pathway. , 2010, Annual review of biochemistry.

[40]  D. Adams,et al.  53BP1 loss rescues BRCA1 deficiency and is associated with triple-negative and BRCA-mutated breast cancers , 2010, Nature Structural &Molecular Biology.

[41]  Jeremy M. Stark,et al.  53BP1 Inhibits Homologous Recombination in Brca1-Deficient Cells by Blocking Resection of DNA Breaks , 2010, Cell.

[42]  M. Jasin,et al.  Mitotic homologous recombination maintains genomic stability and suppresses tumorigenesis , 2010, Nature Reviews Molecular Cell Biology.

[43]  Linda Z. Shi,et al.  CtIP links DNA double-strand break sensing to resection. , 2009, Molecular cell.

[44]  D. Baird,et al.  Fusion of short telomeres in human cells is characterized by extensive deletion and microhomology, and can result in complex rearrangements , 2009, Nucleic acids research.

[45]  J. Murnane,et al.  Increased sensitivity of subtelomeric regions to DNA double-strand breaks in a human cancer cell line. , 2009, DNA repair.

[46]  Ralph Scully,et al.  Role of mammalian Mre11 in classical and alternative non-homologous end joining , 2009, Nature Structural &Molecular Biology.

[47]  D. Ferguson,et al.  Multiple functions of MRN in end-joining pathways during isotype class switching , 2009, Nature Structural &Molecular Biology.

[48]  P. Jeggo,et al.  The impact of heterochromatin on DSB repair. , 2009, Biochemical Society transactions.

[49]  D. Delia,et al.  The Shelterin Protein TRF2 Inhibits Chk2 Activity at Telomeres in the Absence of DNA Damage , 2009, Current Biology.

[50]  B. Shiotani,et al.  Single-stranded DNA orchestrates an ATM-to-ATR switch at DNA breaks. , 2009, Molecular cell.

[51]  Wilhelm Palm,et al.  How shelterin protects mammalian telomeres. , 2008, Annual review of genetics.

[52]  Jeremy M. Stark,et al.  Alternative-NHEJ Is a Mechanistically Distinct Pathway of Mammalian Chromosome Break Repair , 2008, PLoS genetics.

[53]  Shunichi Takeda,et al.  Ctp1/CtIP and the MRN complex collaborate in the initial steps of homologous recombination. , 2007, Molecular cell.

[54]  T. Lange,et al.  Protection of telomeres through independent control of ATM and ATR by TRF2 and POT1 , 2007, Nature.

[55]  Gaudenz Danuser,et al.  Positional stability of single double-strand breaks in mammalian cells , 2007, Nature Cell Biology.

[56]  M. Honma,et al.  Non-homologous end-joining for repairing I-SceI-induced DNA double strand breaks in human cells. , 2007, DNA repair.

[57]  T. Date,et al.  53BP1 contributes to survival of cells irradiated with X‐ray during G1 without Ku70 or Artemis , 2006, Genes to cells : devoted to molecular & cellular mechanisms.

[58]  Y. Taniguchi,et al.  Genetic dissection of vertebrate 53BP1: a major role in non-homologous end joining of DNA double strand breaks. , 2006, DNA repair.

[59]  T. Varga,et al.  Chromosomal aberrations induced by double strand DNA breaks. , 2005, DNA repair.

[60]  C. Azzalin,et al.  New mammalian cellular systems to study mutations introduced at the break site by non-homologous end-joining. , 2005, DNA repair.

[61]  Martin Kühne,et al.  A pathway of double-strand break rejoining dependent upon ATM, Artemis, and proteins locating to gamma-H2AX foci. , 2004, Molecular cell.

[62]  Jiri Bartek,et al.  53BP1 functions in an ATM-dependent checkpoint pathway that is constitutively activated in human cancer , 2002, Nature Cell Biology.

[63]  J. Murnane,et al.  Chromosome Instability as a Result of Double-Strand Breaks near Telomeres in Mouse Embryonic Stem Cells , 2002, Molecular and Cellular Biology.

[64]  T. Lange.  Protection of mammalian telomeres , 2002, Oncogene.

[65]  W. Goedecke,et al.  Mechanisms of DNA double-strand break repair and their potential to induce chromosomal aberrations. , 2000, Mutagenesis.

[66]  W. Lutz,et al.  On the role of DNA double-strand breaks in toxicity and carcinogenesis. , 1997, Critical reviews in toxicology.

[67]  P. Jeggo,et al.  DNA double-strand break repair and V(D)J recombination: involvement of DNA-PK. , 1995, Trends in biochemical sciences.

[68]  P. Sung.  Catalysis of ATP-dependent homologous DNA pairing and strand exchange by yeast RAD51 protein. , 1994, Science.

[69]  J. Haber,et al.  Characterization of double-strand break-induced recombination: homology requirements and single-stranded DNA formation , 1992, Molecular and cellular biology.

[70]  G. Iliakis,et al.  Kinetics of DNA double-strand break repair throughout the cell cycle as assayed by pulsed field gel electrophoresis in CHO cells. , 1991, International journal of radiation biology.

[71]  A. D’Andrea,et al.  Repair Pathway Choices and Consequences at the Double-Strand Break. , 2016, Trends in cell biology.

[72]  Yu Zhang,et al.  An essential role for CtIP in chromosomal translocation formation through an alternative end-joining pathway , 2011, Nature Structural &Molecular Biology.

[73]  C. Badie,et al.  Hypersensitivity of ataxia telangiectasia fibroblasts to ionizing radiation is associated with a repair deficiency of DNA double-strand breaks. , 1997, International journal of radiation biology.

[74]  Open access, freely available online PLoS BIOLOGY The Telomeric Protein TRF2 Binds the ATM Kinase and Can Inhibit the ATM-Dependent DNA Damage Response , 2022 .