Akt and 14-3-3η regulate Miz1 to control cell-cycle arrest after DNA damage
Copyright policy )Akt and 14-3-3η regulate Miz1 to control cell-cycle arrest after DNA damage
The transcription factor Miz1 is required for DNA-damage-induced cell-cycle arrest. We have now identified 14-3-3eta as a gene that inhibits Miz1 function through interaction with its DNA binding domain. Binding of 14-3-3eta 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 14-3-3eta; second, Miz1 represses the expression of many genes in response to DNA damage in an Akt- and 14-3-3eta-regulated manner.
- Antoni van Leeuwenhoek Hospital Netherlands
- Netherlands Heart Institute Netherlands
- Philipps-University of Marburg Germany
- Friedrich Miescher Institute Switzerland
- Novartis (Switzerland) Switzerland
Cell Cycle, Molecular Sequence Data, Kruppel-Like Transcription Factors, Cell Cycle Proteins, Protein Serine-Threonine Kinases, Protein Structure, Tertiary, DNA-Binding Proteins, Mice, 14-3-3 Proteins, Gene Expression Regulation, Proto-Oncogene Proteins, NIH 3T3 Cells, Animals, Humans, Phosphorylation, Proto-Oncogene Proteins c-akt, DNA Damage, Gene Library, HeLa Cells, Protein Binding
Cell Cycle, Molecular Sequence Data, Kruppel-Like Transcription Factors, Cell Cycle Proteins, Protein Serine-Threonine Kinases, Protein Structure, Tertiary, DNA-Binding Proteins, Mice, 14-3-3 Proteins, Gene Expression Regulation, Proto-Oncogene Proteins, NIH 3T3 Cells, Animals, Humans, Phosphorylation, Proto-Oncogene Proteins c-akt, DNA Damage, Gene Library, HeLa Cells, Protein Binding
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