非表示:
キーワード:
NUCLEOTIDE EXCISION-REPAIR; HOMOLOGOUS RECOMBINATION; TOPOISOMERASE-I;
BIOLOGICAL CONSEQUENCES; RAD32(MRE11) NUCLEASE; HISTONE DEMETHYLATION;
GENOMIC INSTABILITY; INDUCED MUTAGENESIS; DAMAGE RESPONSE; CELLS
DEFICIENT
要旨:
DNA-protein crosslinks (DPCs) are highly toxic DNA adducts, but whether dedicated DPC-repair mechanisms exist was until recently unknown. This has changed with discoveries made in yeast and Xenopus laevis that revealed a protease-based DNA-repair pathway specific for DPCs. Importantly, mutations in the gene encoding the putative human homologue of a yeast DPC protease cause a human premature ageing and cancer predisposition syndrome. Thus, DPC repair is a previously overlooked genome-maintenance mechanism that may be essential for tumour suppression.
