Threonine 68 is required for radiation-induced phosphorylation and activation of Cds1.

摘要: In response to DNA damage, eukaryotic cells use a system of checkpoint controls delay cell-cycle progression. Checkpoint delays provide time for repair damaged before its replication in S phase and segregation chromatids M phase1. The Cds1 (Chk2) tumour-suppressor protein2 has been implicated certain responses mammalian cells. It directly phosphorylates inactivates the mitosis-inducing phosphatase Cdc25 vitro is required maintain G2 arrest that observed γ-irradiation3,4,5. also p53 at site stabilization, stabilization induction p53-dependent transcripts vivo upon γ-ionizing radiation5,6,7. Thus, functions both G1 responses. Like Cds1, protein kinase ATM (ataxia-telangiectasia-mutated) correct operation damage checkpoints. necessary phosphorylation activation vivo4 can phosphorylate vitro8, although evidence sites are phosphorylated by lacking. Here we show threonine 68 preferred vitro, principal irradiation-induced vivo. importance this demonstrated failure mutant, non-phosphorylatable form be fully activated, reduced ability induce ionising radiation.