The potential roles of p53 tumor suppressor in nucleotide excision repair (NER) and base excision repair (BER).
The p53 tumor suppressor has long been envisaged to preserve genetic stability by the induction of cell cycle checkpoints and apoptosis. More recently, p53 has been implicated to play roles in DNA repair responses to genotoxic stresses. UV-damage and the damage caused by certain chemotherapeutics including cisplatin and nitrogen mustards are known to be repaired by the nucleotide excision repair (NER) pathway which is reportedly regulated by p53 and its downstream genes. There are evidences to suggest that the base excision repair (BER) induced by the base-damaging agent methyl methanesulfonate (MMS) is partially deficient in cells lacking functional p53. This result suggests that the activity of BER might be also dependent on the p53 status. In this review, we discuss the possibilities that p53 regulates BER as well as NER; these are one of the most significant potentials of p53 tumor suppressor for repairing the vast majority of DNA damages that is incurred from various environmental stresses.
Seo
Young Rok
YR
Department of Pharmacology, Institute for Basic Medical Science (IBMS), College of Medicine, Kyung Hee University, Dongdaemun-gu, Seoul 130-701, South Korea. dream21@khu.ac.kr
Jung
Hwa Jin
HJ
D000818:Animals; D000970:Antineoplastic Agents / Q000494:pharmacology; D004247:DNA / Q000187:drug effects; D004249:DNA Damage; D004260:DNA Repair / Q000502:physiology*; D006801:Humans; D051379:Mice; D016159:Tumor Suppressor Protein p53 / Q000502:physiology*
D000970:Antineoplastic Agents; D016159:Tumor Suppressor Protein p53; D004247:DNA