Article abstract
Nature Cell Biology 7, 30 - 41 (2004)
Published online: 5 December 2004 | doi:10.1038/ncb1202
Akt and 14-3-3
regulate Miz1 to control cell-cycle arrest after DNA damage
Michael Wanzel1,4, Daniela Kleine-Kohlbrecher1,4, Steffi Herold1,4, Andreas Hock1, Katrien Berns2, Jongsun Park3, Brian Hemmings3 & Martin Eilers1
Abstract
The transcription factor Miz1 is required for DNA-damage-induced cell-cycle arrest. We have now identified 14-3-3
as a gene that inhibits Miz1 function through interaction with its DNA binding domain. Binding of 14-3-3 to Miz1 depends on phosphorylation by Akt and regulates the recovery of cells from arrest after DNA damage. Miz1 has two functions in response to DNA damage: first, it is required for upregulation of a large group of genes, a function that is regulated by c-Myc, but not by 14-3-3; second, Miz1 represses the expression of many genes in response to DNA damage in an Akt- and 14-3-3-regulated manner.
- Institute for Molecular Biology and Tumor Research (IMT), University of Marburg, Emil-Mannkopff-Strasse 2, 35033 Marburg, Germany.
- Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX Amsterdam, Netherlands.
- Friedrich Miescher Institute, Novartis Research Foundation, Maulbeerstrasse 66, CH 4058- Basel, Switzerland.
- These authors contributed equally to this work.
Correspondence to: Martin Eilers1 e-mail: eilers@imt.uni-marburg.de
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