14-3-3c mediates Cdc25A proteolysis to block premature mitotic entry after DNA damage
نویسندگان
چکیده
Kousuke Kasahara, Hidemasa Goto, Masato Enomoto, Yasuko Tomono, Tohru Kiyono and Masaki Inagaki* Division of Biochemistry, Aichi Cancer Center Research Institute, Nagoya, Aichi, Japan, Department of Cellular Oncology, Nagoya University Graduate School of Medicine, Nagoya, Aichi, Japan, Division of Molecular and Cell Biology, Shigei Medical Research Institute, Okayama, Okayama, Japan and Virology Division, National Cancer Center Research Institute, Chuo-ku, Tokyo, Japan
منابع مشابه
14-3-3gamma mediates Cdc25A proteolysis to block premature mitotic entry after DNA damage.
14-3-3 proteins control various cellular processes, including cell cycle progression and DNA damage checkpoint. At the DNA damage checkpoint, some subtypes of 14-3-3 (beta and zeta isoforms in mammalian cells and Rad24 in fission yeast) bind to Ser345-phosphorylated Chk1 and promote its nuclear retention. Here, we report that 14-3-3gamma forms a complex with Chk1 phosphorylated at Ser296, but n...
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The ability to inappropriately progress through S phase during drug treatment is a key determinant of tumor cell sensitivity to thymidylate synthase inhibitors such as 5-fluoro-2'-deoxyuridine (FdUrd). Previous studies suggest that SW620 cells, which are relatively resistant to FdUrd, have an intact early S-phase checkpoint that protects against FdUrd-induced DNA damage and cytotoxicity and tha...
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The order and fidelity of cell cycle events in mammals is intimately linked to the integrity of the Chk1 kinase-Cdc25A phosphatase pathway. Chk1 phosphorylation targets Cdc25A for destruction and, as shown here, inhibits interactions between Cdc25A and its mitotic substrate cyclin B1-Cdk1. Phosphorylation of Cdc25A on serine 178 and threonine 507 facilitates 14-3-3 binding, and Chk1 phosphoryla...
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Shelterin component TRF2 prevents ATM activation, while POT1 represses ATR signalling at telomeres. Here, we investigate the mechanism of G2/M arrest triggered by telomeres uncapped through TRF2 or POT1 inhibition in human cells. We find that telomere damage-activated ATR and ATM phosphorylate p53, as well as CHK1 and CHK2, thus activating two independent pathways to prevent progression into mi...
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تاریخ انتشار 2010