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    Repair of dihydrouracil supported by base excision repair in mNTH1 knock-out cell extracts.

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    Authors
    Elder, Rhoderick H
    Dianov, Grigory L
    Affiliation
    Medical Research Council Radiation and Genome Stability Unit, Harwell, Oxfordshire, OX11 0RD, United Kingdom.
    Issue Date
    2002-12-27
    
    Metadata
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    Abstract
    In mammalian cells, thymine glycols and other oxidized pyrimidines such as 5,6-dihydrouracil are removed from DNA by the NTH1 protein, a bifunctional DNA-N-glycosylase. However, mNTH1 knock-out mice in common with other DNA glycosylase-deficient mice do not show any severe abnormalities associated with accumulation of DNA damage and mutations. In the present study we used an in vitro repair system to investigate the mechanism for the removal of 5,6-dihydrouracil from DNA by mNTH1-deficient cell-free extracts derived from testes of mNTH1 knock-out mice. We found that these extracts are able to support the removal of 5,6-dihydrouracil from DNA at about 20% of the efficiency of normal extracts. Furthermore, we also found that single-nucleotide patch base excision repair is the major pathway for removal of 5,6-dihydrouracil in mNTH1-deficient cell extracts, suggesting the involvement of other DNA glycosylase(s) in the removal of oxidized pyrimidines.
    Citation
    Repair of dihydrouracil supported by base excision repair in mNTH1 knock-out cell extracts. 2002, 277 (52):50487-90 J. Biol. Chem.
    Journal
    The Journal of Biological Chemistry
    URI
    http://hdl.handle.net/10541/83548
    DOI
    10.1074/jbc.M208153200
    PubMed ID
    12401779
    Type
    Article
    Language
    en
    ISSN
    0021-9258
    ae974a485f413a2113503eed53cd6c53
    10.1074/jbc.M208153200
    Scopus Count
    Collections
    All Paterson Institute for Cancer Research

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