Nuclear localization of Cdc25 is regulated by DNA damage and a 14-3-3 protein
作者： Antonia Lopez-Girona , Beth Furnari , Odile Mondesert , Paul Russell
DOI: 10.1038/16488
关键词: Mitosis 、 Biology 、 DNA damage 、 Cell cycle checkpoint 、 G2-M DNA damage checkpoint 、 DNA repair 、 Nuclear export signal 、 Cell biology 、 CHEK1 、 Biochemistry 、 Nuclear localization sequence
摘要: DNA damage activates a cell-cycle checkpoint that prevents mitosis while repair is under way. The protein Chk1 enforces this by phosphorylating the mitotic inducer Cdc25. Phosphorylation of Cdc25 creates binding site in for 14-3-3 proteins, but it not known how proteins regulate Rad24 important DNA-damage fission yeast. Here we show controls intracellular distribution Elimination causes nuclear accumulation Activation net export process requires Chk1, and nuclear-export machinery. Mutation putative signal impairs exclusion Rad24, damage-induced checkpoint. Thus, appears to function as an attachable enhances response damage.
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