The arrest at G1/S checkpoint is mediated by the action of a widely known tumor suppressor protein, p53. Loss of p53 functions, as a result of mutations in cancer prevent the G1/S checkpoint (Kuerbitz et al, 1992). P53 is rapidly induced in response to damaged DNA. A number of kinases, phosphatases, histone acetylases and ubiquitin-conjugating enzymes regulate the stability as well as transcriptional activity of p53 after DNA damage.
Kastan, MB, Kuerbitz, SJ, Plunkett, BS, Walsh, WV
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