A role for ATR in the DNA damage-induced phosphorylation of p53
Copyright policy )A role for ATR in the DNA damage-induced phosphorylation of p53
Phosphorylation at Ser-15 may be a critical event in the up-regulation and functional activation of p53 during cellular stress. In this report we provide evidence that the ATM-Rad3-related protein ATR regulates phosphorylation of Ser-15 in DNA-damaged cells. Overexpression of catalytically inactive ATR (ATRki) in human fibroblasts inhibited Ser-15 phosphorylation in response to gamma-irradiation and UV light. In gamma-irradiated cells, ATRki expression selectively interfered with late-phase Ser-15 phosphorylation, whereas ATRki blocked UV-induced Ser-15 phosphorylation in a time-independent manner. ATR phosphorylated p53 at Ser-15 and Ser-37 in vitro, suggesting that p53 is a target for phosphorylation by ATR in DNA-damaged cells.
- King’s University United States
- Columbia University United States
- Duke University United States
- Mayo Clinic United States
Time Factors, Recombinant Fusion Proteins, Proteins, Cell Cycle Proteins, Ataxia Telangiectasia Mutated Proteins, Fibroblasts, Protein Serine-Threonine Kinases, Transfection, Precipitin Tests, DNA-Binding Proteins, Gamma Rays, Doxycycline, Mutation, Serine, Tumor Cells, Cultured, Humans, Phosphorylation, Tumor Suppressor Protein p53, K562 Cells, DNA Damage
Time Factors, Recombinant Fusion Proteins, Proteins, Cell Cycle Proteins, Ataxia Telangiectasia Mutated Proteins, Fibroblasts, Protein Serine-Threonine Kinases, Transfection, Precipitin Tests, DNA-Binding Proteins, Gamma Rays, Doxycycline, Mutation, Serine, Tumor Cells, Cultured, Humans, Phosphorylation, Tumor Suppressor Protein p53, K562 Cells, DNA Damage
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