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Deborah E. Barnes
Researcher at London Research Institute
Publications - 40
Citations - 9461
Deborah E. Barnes is an academic researcher from London Research Institute. The author has contributed to research in topics: DNA repair & DNA ligase. The author has an hindex of 32, co-authored 39 publications receiving 9029 citations. Previous affiliations of Deborah E. Barnes include Guy's and St Thomas' NHS Foundation Trust & University of Cambridge.
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Journal ArticleDOI
Reconstitution of DNA base excision-repair with purified human proteins: interaction between DNA polymerase beta and the XRCC1 protein.
TL;DR: Data indicate that XRCC1, which has no known catalytic activity, might serve as a scaffold protein during base excision‐repair, allowing for more efficient ligation after filling of a single nucleotide patch.
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Accumulation of premutagenic dna lesions in mice defective in removal of oxidative base damage
Arne Klungland,Ian Rosewell,Stephan Hollenbach,Elisabeth Larsen,Graham Daly,Bernd Epe,Erling Seeberg,Tomas L. Lindahl,Deborah E. Barnes +8 more
TL;DR: Findings suggest that in the absence of the DNA glycosylase, and in apparent contrast to bacterial and yeast cells, an alternative repair pathway functions to minimize the effects of an increased load of 8-oxoG in the genome and maintain a low endogenous mutation frequency.
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Mutations in the gene encoding the 3'-5' DNA exonuclease TREX1 cause Aicardi-Goutières syndrome at the AGS1 locus.
Yanick J. Crow,Yanick J. Crow,Bruce E. Hayward,Rekha Parmar,Peter Robins,Andrea Leitch,Manir Ali,Deborah N. Black,Hans van Bokhoven,Han G. Brunner,Ben C.J. Hamel,Peter Corry,Frances M. Cowan,S Frints,Joerg Klepper,John H. Livingston,Sally Ann Lynch,Roger F. Massey,Jean François Meritet,Jacques L. Michaud,Gérard Ponsot,Thomas Voit,Pierre Lebon,David T. Bonthron,Andrew P. Jackson,Deborah E. Barnes,Tomas Lindahl +26 more
TL;DR: TREX1, encoding the major mammalian 3′ → 5′ DNA exonuclease, is the AGS1 gene, and AGS-causing mutations result in abrogation of TREX1 enzyme activity, and failure of which results in the triggering of an abnormal innate immune response.
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Immunoglobulin Isotype Switching Is Inhibited and Somatic Hypermutation Perturbed in UNG-Deficient Mice
Cristina Rada,Gareth T. Williams,Hilde Nilsen,Deborah E. Barnes,Tomas L Lindahl,Michael S. Neuberger +5 more
TL;DR: The results provide strong support for the DNA deamination model for antibody diversification with respect to class-switching as well as hypermutation and suggest that UNG is the major mouse DNA glycosylase responsible for processing the programmed dU/dG lesions within the immunoglobulin locus.
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Repair and Genetic Consequences of Endogenous DNA Base Damage in Mammalian Cells
Deborah E. Barnes,Tomas Lindahl +1 more
TL;DR: Repairs of endogenous DNA base damage by the ubiquitous base-excision repair pathway largely accounts for the significant turnover of DNA even in nonreplicating cells, and must be sufficiently accurate and efficient to preserve genome stability compatible with long-term cellular viability.