The SNM1A DNA repair nuclease.

Autor: Baddock HT; Department of Oncology, MRC Weatherall Institute of Molecular Medicine, University of Oxford, OX3 9DS, UK., Yosaatmadja Y; Structural Genomics Consortium, University of Oxford, OX3 7DQ, UK., Newman JA; Chemistry Research Laboratory, University of Oxford, 12 Mansfield Road, OX1 3TA, UK., Schofield CJ; Chemistry Research Laboratory, University of Oxford, 12 Mansfield Road, OX1 3TA, UK., Gileadi O; Structural Genomics Consortium, University of Oxford, OX3 7DQ, UK., McHugh PJ; Department of Oncology, MRC Weatherall Institute of Molecular Medicine, University of Oxford, OX3 9DS, UK. Electronic address: peter.mchugh@imm.ox.ac.uk.
Jazyk: angličtina
Zdroj: DNA repair [DNA Repair (Amst)] 2020 Nov; Vol. 95, pp. 102941. Date of Electronic Publication: 2020 Jul 31.
DOI: 10.1016/j.dnarep.2020.102941
Abstrakt: Unrepaired, or misrepaired, DNA damage can contribute to the pathogenesis of a number of conditions, or disease states; thus, DNA damage repair pathways, and the proteins within them, are required for the safeguarding of the genome. Human SNM1A is a 5'-to-3' exonuclease that plays a role in multiple DNA damage repair processes. To date, most data suggest a role of SNM1A in primarily ICL repair: SNM1A deficient cells exhibit hypersensitivity to ICL-inducing agents (e.g. mitomycin C and cisplatin); and both in vivo and in vitro experiments demonstrate SNM1A and XPF-ERCC1 can function together in the 'unhooking' step of ICL repair. SNM1A further interacts with a number of other proteins that contribute to genome integrity outside canonical ICL repair (e.g. PCNA and CSB), and these may play a role in regulating SNM1As function, subcellular localisation, and post-translational modification state. These data also provide further insight into other DNA repair pathways to which SNM1A may contribute. This review aims to discuss all aspects of the exonuclease, SNM1A, and its contribution to DNA damage tolerance.
(Crown Copyright © 2020. Published by Elsevier B.V. All rights reserved.)
Databáze: MEDLINE
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