DNA double-strand break repair pathway choice and cancer

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53BP1 Inhibits Homologous Recombination in Brca1-Deficient Cells by Blocking Resection of DNA Breaks

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Repair of Strand Breaks by Homologous RecombinationPreprint

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Alternative-NHEJ Is a Mechanistically Distinct Pathway of Mammalian Chromosome Break Repair

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BLM–DNA2–RPA–MRN and EXO1–BLM–RPA–MRN constitute two DNA end resection machineries for human DNA break repairPreprint

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Defying death after DNA damage

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DNA end resection, homologous recombination and DNA damage checkpoint activation require CDK1

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RIF1 Is Essential for 53BP1-Dependent Nonhomologous End Joining and Suppression of DNA Double-Strand Break Resection

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53BP1 Regulates DSB Repair Using Rif1 to Control 5′ End Resection

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DNA Double-Strand Break Repair Pathway Choice Is Directed by Distinct MRE11 Nuclease Activities

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CtIP-BRCA1 modulates the choice of DNA double-strand-break repair pathway throughout the cell cycle

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Human CtIP Mediates Cell Cycle Control of DNA End Resection and Double Strand Break Repair

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The Fanconi Anemia Pathway Promotes Replication-Dependent DNA Interstrand Cross-Link Repair

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Ku DNA end-binding protein modulates homologous repair of double-strand breaks in mammalian cellsPreprint

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Factors determining DNA double‐strand break repair pathway choice in G2 phase

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CDK targets Sae2 to control DNA-end resection and homologous recombination

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Modernizing the Nonhomologous End-Joining Repertoire: Alternative and Classical NHEJ Share the Stage

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Cell Cycle-dependent Complex Formation of BRCA1·CtIP·MRN Is Important for DNA Double-strand Break Repair

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A forward chemical genetic screen reveals an inhibitor of the Mre11–Rad50–Nbs1 complex

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Rif1 Prevents Resection of DNA Breaks and Promotes Immunoglobulin Class Switching

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The CDK regulates repair of double‐strand breaks by homologous recombination during the cell cycle

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53BP1: pro choice in DNA repair

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The neurodegenerative disease protein aprataxin resolves abortive DNA ligation intermediates

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Yeast Gene for a Tyr-DNA Phosphodiesterase that Repairs Topoisomerase I Complexes

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Role of Mre11 in chromosomal nonhomologous end joining in mammalian cells

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The nonhomologous end-joining pathway of DNA repair is required for genomic stability and the suppression of translocations

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Mutations in ERCC4, encoding the DNA-repair endonuclease XPF, cause Fanconi anemia.

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A Selective Requirement for 53BP1 in the Biological Response to Genomic Instability Induced by Brca1 Deficiency

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Ku prevents Exo1 and Sgs1‐dependent resection of DNA ends in the absence of a functional MRX complex or Sae2

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Preventing Nonhomologous End Joining Suppresses DNA Repair Defects of Fanconi Anemia

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Molecular Cloning of the Human Gene, PNKP, Encoding a Polynucleotide Kinase 3′-Phosphatase and Evidence for Its Role in Repair of DNA Strand Breaks Caused by Oxidative Damage

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An essential role for CtIP in chromosomal translocation formation through an alternative end-joining pathway

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RIF1 Counteracts BRCA1-mediated End Resection during DNA Repair

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RPA Coordinates DNA End Resection and Prevents Formation of DNA Hairpins

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Ku70 Corrupts DNA Repair in the Absence of the Fanconi Anemia Pathway

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ATM and the Molecular Pathogenesis of Ataxia Telangiectasia

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BRCA1 tumor suppression depends on BRCT phosphoprotein binding, but not its E3 ligase activity

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A Critical Role for the Ubiquitin-Conjugating Enzyme Ubc13 in Initiating Homologous Recombination

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Alternative end-joining catalyzes robust IgH locus deletions and translocations in the combined absence of ligase 4 and Ku70

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Ku is a 5′-dRP/AP lyase that excises nucleotide damage near broken ends

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Differential Regulation of the Cellular Response to DNA Double-Strand Breaks in G1

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Collaborative Action of Brca1 and CtIP in Elimination of Covalent Modifications from Double-Strand Breaks to Facilitate Subsequent Break Repair

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A novel human AP endonuclease with conserved zinc‐finger‐like motifs involved in DNA strand break responses

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DNA end resection by CtIP and exonuclease 1 prevents genomic instability

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Alternative end-joining mechanisms: a historical perspective

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Exo1 plays a major role in DNA end resection in humans and influences double-strand break repair and damage signaling decisions

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The Role of Mechanistic Factors in Promoting Chromosomal Translocations Found in Lymphoid and Other Cancers

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Recruitment and Dissociation of Nonhomologous End Joining Proteins at a DNA Double-Strand Break in Saccharomyces cerevisiae

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Links between genome integrity and BRCA1 tumor suppression

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Controlling DNA-end resection: a new task for CDKs

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Double-strand break repair by homologous recombination in primary mouse somatic cells requires BRCA1 but not the ATM kinase

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Functional Interplay of the Mre11 Nuclease and Ku in the Response to Replication-Associated DNA Damage

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BRCA1 Promotes Induction of ssDNA by Ionizing Radiation

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Werner Syndrome Helicase Has a Critical Role in DNA Damage Responses in the Absence of a Functional Fanconi Anemia Pathway

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The interaction between CtIP and BRCA1 is not essential for resection-mediated DNA repair or tumor suppression

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Cdk1 uncouples CtIP-dependent resection and Rad51 filament formation during M-phase double-strand break repair

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Limiting the Persistence of a Chromosome Break Diminishes Its Mutagenic Potential

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Fanconi anemia proteins stabilize replication forks

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Deficient DNA End Joining Activity in Extracts from Fanconi Anemia Fibroblasts

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Live imaging of induced and controlled DNA double-strand break formation reveals extremely low repair by homologous recombination in human cells

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Regulation of repair choice: Cdk1 suppresses recruitment of end joining factors at DNA breaks

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Alternative Pathways for the Repair of RAG-Induced DNA Breaks

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The Basal Phenotype of BRCA1-Related Breast Cancer: Past, Present and Future

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The Fanconi anemia pathway limits the severity of mutagenesis

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Mouse models for BRCA1 associated tumorigenesis: From fundamental insights to preclinical utility

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Trimming of damaged 3′ overhangs of DNA double-strand breaks by the Metnase and Artemis endonucleases

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Analysis of MRE11's function in the 5'->3' processing of DNA double-strand breaks

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