Regular ArticleProtein kinases and the response to DNA damage
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Nitric oxide prevents UV-induced phosphorylation of the p53 tumor-suppressor protein at serine 46: A possible role in inhibition of apoptosis
2003, Biochemical and Biophysical Research CommunicationsCitation Excerpt :This inhibitor strongly suppressed the UV-induced phosphorylation of the kinase substrates (ATM/ATR substrates and akt) (Fig. 3B). Since in UV-irradiated cells only ATR, but not ATM, plays a major role in p53 phosphorylation [25–28], increased phosphorylation of ATM/ATR kinase substrate upon UV irradiation is considered to be mediated by increased activity of ATR kinase. Treatment with L-JNK1, the JNK specific inhibitor, did not affect the UV-induced p53 phosphorylation at Ser-15 and Ser-46 (Fig. 3C).
Cellular responses to the DNA strand-scission enediyne C-1027 can be independent of ATM, ATR, and DNA-PK kinases
2002, Journal of Biological ChemistryTranscriptional effects of the potent enediyne anti-cancer agent calicheamicin γ<inf>1</inf><sup>I</sup>
2002, Chemistry and BiologyHuman p53 is phosphorylated on serines 6 and 9 in response to DNA damage-inducing agents
2000, Journal of Biological ChemistryCitation Excerpt :However, the peptide p53(Ac-1–12)(6P), was readily phosphorylated by CK1-δ. The response of mammalian cells to DNA damage is complex (reviewed in Refs. 24-26). Cell cycle progression is controlled by several checkpoints that are activated by DNA damage, by other stresses, and by mechanisms that ensure the orderly progression of cell cycle events.
Post-translational modification of p53 protein in response to ionizing radiation analyzed by mass spectrometry
2000, Journal of Molecular BiologyMultisite phosphorylation and the integration of stress signals at p53
1998, Cellular Signalling