Cell-cycle-dependent and ATM-independent expression of human Chk1 kinase.

摘要: Checkpoint genes cause cell cycle arrest when DNA is damaged or replication blocked. Although a human homolog of Chk1 (hChk1) has recently been reported to be involved in the damage checkpoint through phosphorylation Cdc25A, B, and C, it not known at which phase(s) hChk1 functions how causes response damage. In present study, we demonstrate that normal fibroblasts (MJ90), expressed specifically S M phase both RNA protein levels localized nucleus this time. activity, as determined by Cdc25C, readily detected cycle, induced UV ionizing radiation does enhance expression its activity. Furthermore, exists an active form derived from patients with ataxia telangiectasia (AT) lack functional AT mutated (ATM) gene product, suggesting independent ATM. Taken together findings Cdc25C on serine 216 increased phase, suggested particular even absence damage, phosphorylates 216, considered prerequisite for G2/M checkpoint. Thus, may play important role keeping prepared responding phosphorylating residue during phase.