Abstract：
:Activation of p53 by DNA damage results in either cell-cycle arrest, allowing DNA repair and cell survival, or induction of apoptosis. As these opposite outcomes are both mediated by p53 stabilization, additional mechanisms to determine this decision must exist. Here, we show that glycogen synthase kinase-3 (GSK-3) is required for the p53-mediated induction of the proapoptotic BH3 only-protein PUMA, an essential mediator of p53-induced apoptosis. Inhibition of GSK-3 protected from cell death induced by DNA damage and promoted increased long-term cell survival. We demonstrate that GSK-3 phosphorylates serine 86 of the p53-acetyltransferase Tip60. A Tip60(S86A) mutant was less active to induce p53 K120 acetylation, histone 4 acetylation, and expression of PUMA. Our data suggest that GSK-3 mediated Tip60S86 phosphorylation provides a link between PI3K signaling and the choice for or against apoptosis induction by p53.
journal_name
Mol Celljournal_title
Molecular cellauthors
Charvet C,Wissler M,Brauns-Schubert P,Wang SJ,Tang Y,Sigloch FC,Mellert H,Brandenburg M,Lindner SE,Breit B,Green DR,McMahon SB,Borner C,Gu W,Maurer Udoi
10.1016/j.molcel.2011.03.033subject
Has Abstractpub_date
2011-06-10 00:00:00pages
584-96issue
5eissn
1097-2765issn
1097-4164pii
S1097-2765(11)00343-1journal_volume
42pub_type
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