Chk1 phosphorylation during mitosis: a new role for a master regulator.
The human DNA damage responses are modulated by both nonessential and essential pathways. The extensively studied ATM kinase and p53 are examples of the former. While loss-of-function mutations in genes that encode ATM and p53 cause marked predispositions to cancer, the loss of these proteins does not appear to impact basic cell growth and proliferation. In contrast, the checkpoint kinase Chk1 and its upstream activator ATR are essential.(1-4) What do these proteins do in undamaged cells?
Wilsker
Deborah
D
Department of Radiation Oncology and Molecular Radiation Sciences, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Bunz
Fred
F
D000818:Animals; D016203:CDC2 Protein Kinase / Q000378:metabolism; D000071877:Checkpoint Kinase 1; D004261:DNA Replication; D006801:Humans; D008938:Mitosis; D010766:Phosphorylation; D011494:Protein Kinases / Q000378:metabolism*; D017346:Protein Serine-Threonine Kinases / Q000378:metabolism; D020687:cdc25 Phosphatases / Q000378:metabolism
D011494:Protein Kinases; C000605867:CHEK1 protein, human; D000071877:Checkpoint Kinase 1; D017346:Protein Serine-Threonine Kinases; D016203:CDC2 Protein Kinase; D020687:cdc25 Phosphatases