Nakano Toshiaki, Salem Amir M H, Terato Hiroaki, Pack Seung Pil, Makino Keisuke, Ide Hiroshi
Department of Mathematical and Life Sciences, Graduate School of Science, Hiroshima University, Higashi-Hiroshima 739-8526, Japan.
Nucleic Acids Symp Ser (Oxf). 2009(53):225-6. doi: 10.1093/nass/nrp113.
Endogenous and environmental genotoxic agents produce DNA damage and induce cell death and mutations. The repair mechanisms of base lesions and single and double strand breaks have been well characterized in both prokaryotic and eukaryotic cells. However, the molecular pathways that repair or tolerate DNA-protein crosslinks (DPCs) remains to be largely elucidated. In this study, we constructed DNA substrates containing defined DPCs and assessed the incision activities of prokaryotic and eukaryotic nucleotide excision repair systems for DPCs in vitro.
内源性和环境基因毒性剂会造成DNA损伤,并诱导细胞死亡和突变。原核细胞和真核细胞中碱基损伤以及单链和双链断裂的修复机制已得到充分表征。然而,修复或耐受DNA-蛋白质交联(DPC)的分子途径在很大程度上仍有待阐明。在本研究中,我们构建了含有特定DPC的DNA底物,并在体外评估了原核和真核核苷酸切除修复系统对DPC的切割活性。