J
J. Ross Chapman
Researcher at University of Oxford
Publications - 29
Citations - 6427
J. Ross Chapman is an academic researcher from University of Oxford. The author has contributed to research in topics: Homologous recombination & DNA repair. The author has an hindex of 23, co-authored 29 publications receiving 5381 citations. Previous affiliations of J. Ross Chapman include Harvard University & University of Sussex.
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Journal ArticleDOI
Playing the End Game: DNA Double-Strand Break Repair Pathway Choice
TL;DR: Recent insights are reviewed into the mechanisms that influence the choice between competing DSB repair pathways, how this is regulated during the cell cycle, and how imbalances in this equilibrium result in genome instability.
Journal ArticleDOI
Orchestration of the DNA-Damage Response by the RNF8 Ubiquitin Ligase
Nadine K. Kolas,J. Ross Chapman,Shinichiro Nakada,Jarkko Ylanko,Jarkko Ylanko,Richard Chahwan,Frédéric D. Sweeney,Frédéric D. Sweeney,Stephanie Panier,Megan Mendez,Jan Wildenhain,Timothy M. Thomson,Laurence Pelletier,Laurence Pelletier,Stephen P. Jackson,Daniel Durocher,Daniel Durocher +16 more
TL;DR: The results demonstrate how the DNA-damage response is orchestrated by ATM-dependent phosphorylation of MDC1 and RNF8-mediated ubiquitination and promote the G2/M DNA damage checkpoint and resistance to ionizing radiation.
Journal ArticleDOI
RIF1 Is Essential for 53BP1-Dependent Nonhomologous End Joining and Suppression of DNA Double-Strand Break Resection
J. Ross Chapman,Patricia Barral,Jean-Baptiste Vannier,Valerie Borel,Martin Steger,Antonia Tomás-Loba,Alessandro A. Sartori,Ian R. Adams,Facundo D. Batista,Simon J. Boulton +9 more
TL;DR: Rif1−/− mice are severely compromised for 53BP1-dependent class switch recombination (CSR) and fusion of dysfunctional telomeres and deletion of Rif1 suppresses toxic nonhomologous end joining (NHEJ) induced by PARP inhibition in Brca1-deficient cells.
Journal ArticleDOI
DNA helicases Sgs1 and BLM promote DNA double-strand break resection
TL;DR: It is revealed that in the absence of exonuclease Exo1 activity, deletion or mutation of the Saccharomyces cerevisiae RecQ-family helicase, Sgs1, causes pronounced hypersensitivity to DSB-inducing agents, and it is established that this reflects severely compromised DSB resection, deficient DNA damage signaling, and strongly impaired HR-mediated repair.
Journal ArticleDOI
REV7 counteracts DNA double-strand break resection and affects PARP inhibition
Guotai Xu,J. Ross Chapman,Inger Brandsma,Jingsong Yuan,Martin Mistrik,Peter Bouwman,Jirina Bartkova,Ewa Gogola,Daniël O. Warmerdam,Marco Barazas,Janneke E. Jaspers,Kenji Watanabe,Mark Pieterse,Ariena Kersbergen,Wendy Sol,Patrick H.N. Celie,Philip C. Schouten,Bram van den Broek,Ahmed Salman,Marja Nieuwland,Iris de Rink,Jorma J. de Ronde,Kees Jalink,Simon J. Boulton,Junjie Chen,Dik C. van Gent,Jiri Bartek,Jos Jonkers,Piet Borst,Sven Rottenberg,Sven Rottenberg +30 more
TL;DR: This work shows that loss of REV7 in mouse and human cell lines re-establishes CTIP-dependent end resection of DSBs in BRCA1-deficient cells, leading to HR restoration and PARP inhibitor resistance, which is reversed by ATM kinase inhibition.