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A role for p53 in base excision repair
Author(s) -
Zhou Jianmin,
Ahn Jinwoo,
Wilson Samuel H.,
Prives Carol
Publication year - 2001
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1093/emboj/20.4.914
Subject(s) - biology , base excision repair , transactivation , ap site , dna repair , ap endonuclease , endonuclease , dna damage , microbiology and biotechnology , dna , dna polymerase beta , dna polymerase , genetics , gene , transcription factor
Wild‐type p53 protein can markedly stimulate base excision repair (BER) in vitro , either reconstituted with purified components or in extracts of cells. In contrast, p53 with missense mutations either at hot‐spots in the core domain or within the N‐terminal transactivation domain is defective in this function. Stimulation of BER by p53 is correlated with its ability to interact directly both with the AP endonuclease (APE) and with DNA polymerase β (pol β). Furthermore, p53 stabilizes the interaction between DNA pol β and abasic DNA. Evidence that this function of p53 is physiologically relevant is supported by the facts that BER activity in human and murine cell extracts closely parallels their levels of endogenous p53, and that BER activity is much reduced in cell extracts immunodepleted of p53. These data suggest a novel role for p53 in DNA repair, which could contribute to its function as a key tumor suppressor.