Base excision repair deficient mice lacking the Aag alkyladenine DNA glycosylase

Bevin P. Engelward, Geert Weeda, Michael D. Wyatt, José L.M. Broekhof, Jan De Wit, Ingrid Donker, James M. Allan, Barry Gold, Jan H.J. Hoeijmakers, Leona D. Samson

Onderzoeksoutput: Bijdrage aan tijdschriftArtikelpeer review

208 Citaten (Scopus)

Samenvatting

3-methyladenine (3MeA) DNA glycosylases remove 3MeAs from alkylated DNA to initiate the base excision repair pathway. Here we report the generation of mice deficient in the 3MeA DNA glycosylase encoded by the Aag (Mpg) gear. Alkyladenine DNA glycosylase turns out to be the major DNA glycosylase not only for the cytotoxic 3MeA DNA lesion, but also for the mutagenic 1,N6- ethenoadenine (εA) and hypoxanthine lesions. Aag appears to be the only 3MeA and hypoxanthine DNA glycosylase in liver, testes, kidney, and lung, and the only εA DNA glycosylase in liver, testes, and kidney; another εA DNA glycosylase may be expressed in lung. Although alkyladenine DNA glycosylase has the capacity to remove 8-oxoguanine DNA lesions, it does not appear to be the major glycosylase for 8-oxoguanine repair. Fibroblasts derived from Aag - /- mice are alkylation sensitive, indicating that Aag -/- mice may be similarly sensitive.

Originele taal-2Engels
Pagina's (van-tot)13087-13092
Aantal pagina's6
TijdschriftProceedings of the National Academy of Sciences of the United States of America
Volume94
Nummer van het tijdschrift24
DOI's
StatusGepubliceerd - 25 nov. 1997
Extern gepubliceerdJa

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