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Oncogene. 2000 Oct 12;19(43):5034-7.

Age-dependent spontaneous mutagenesis in Xpc mice defective in nucleotide excision repair.

Author information

1
Department of Radiation Genetics and Chemical Mutagenesis-MGC, Leiden University Medical Center, 2333 AL Leiden, The Netherlands.

Abstract

DNA damages caused by cellular metabolites and environmental agents induce mutations, that may predispose to cancer. Nucleotide excision repair (NER) is a major cellular defence mechanism acting on a variety of DNA lesions. Here, we show that spontaneous mutant frequencies at the Hprt gene increased 30-fold in T-lymphocytes of 1 year old Xpc-/- mice, possessing only functional transcription-coupled repair (TCR). Hprt mutant frequencies in Xpa-/- and Csb-/- mice that both have a defect in this NER subpathway, remained low during ageing. In contrast to current models, the elevated mutation rate in Xpc-/- mice does not lead to an increased tumour incidence or premature ageing. Oncogene (2000) 19, 5034 - 5037.

PMID:
11042691
DOI:
10.1038/sj.onc.1203844
[Indexed for MEDLINE]
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