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RIF1 Is Essential for 53BP1-Dependent Nonhomologous End Joining and Suppression of DNA Double-Strand Break Resection
Authors:J Ross Chapman  Patricia Barral  Jean-Baptiste Vannier  Valérie Borel  Martin Steger  Antonia Tomas-Loba  Alessandro A Sartori  Ian R Adams  Facundo D Batista  Simon J Boulton
Institution:1. DNA Damage Response Laboratory, London Research Institute, Cancer Research UK, Clare Hall, South Mimms, London EN6 3LD, UK;2. Lymphocyte Interaction Group, London Research Institute, Cancer Research UK, 44 Lincoln’s Inn Field, London WC2A 3LY, UK;3. Institute of Molecular Cancer Research, University of Zurich, Winterthurerstrasse 190, 8057 Zurich, Switzerland;4. MRC Human Genetics Unit, MRC Institute of Genetics and Molecular Medicine, University of Edinburgh, Western General Hospital, Crewe Road, Edinburgh EH4 2XU, UK
Abstract:
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  • Highlights? RIF1 is essential for 53BP1-dependent CSR and fusion of dysfunctional telomeres ? BRCA1 antagonizes RIF1 in S phase to prevent error-prone repair by toxic NHEJ ? N-terminal phospho-SQ/TQ domain of 53BP1 interacts with and recruits RIF1 to DSBs ? RIF1 and 53BP1 promote NHEJ in G1 by blocking 5′ end resection of DSBs
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