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Abstract
53BP1 is a key player in non-homologous end joining (NHEJ). Here the authors reveal an important role for the multifunctional homodimeric protein hub dynein light chain 1 (DYNLL1) in increasing the efficacy of 53BP1-mediated repair of DNA double-strand breaks (DSBs) by NHEJ.
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1 Genome Integrity Laboratory, Wellcome Centre for Human Genetics, University of Oxford, Oxford, UK
2 Division of Molecular Pathology, Oncode Institute, The Netherlands Cancer Institute, Amsterdam, The Netherlands
3 St. Vincent’s Institute of Medical Research, Fitzroy, VIC, Australia
4 Genome Damage and Stability Centre, School of Life Sciences, University of Sussex, Falmer, UK
5 MRC Brain Network Dynamics Unit, Department of Pharmacology, University of Oxford, Oxford, UK
6 Department of Oncology, Weatherall Institute of Molecular Medicine, University of Oxford, John Radcliffe Hospital, Oxford, UK; CRUK/MRC Oxford Institute for Radiation Oncology, University of Oxford, Oxford, UK
7 St. Vincent’s Institute of Medical Research, Fitzroy, VIC, Australia; Department of Medicine at St. Vincent’s Hospital, Melbourne Medical School, The University of Melbourne, Fitzroy, VIC, Australia
8 Division of Molecular Pathology, Oncode Institute, The Netherlands Cancer Institute, Amsterdam, The Netherlands; Institute of Animal Pathology, Vetsuisse Faculty, University of Bern, Bern, Switzerland