title: Turning off the G2 DNA damage checkpoint.
abstract: In response to DNA damage, cells activate checkpoints to delay cell cycle progression and allow time for completion of DNA repair before commitment to S-phase or mitosis. During G2, many proteins collaborate to activate Chk1, an effector protein kinase that ensures the mitotic cyclin-dependent kinase remains in an inactive state. This checkpoint is ancient in origin and highly conserved from fission yeast to humans. Work from many groups has led to a detailed description of the spatiotemporal control of signaling events leading to Chk1 activation. However, to survive DNA damage in G2, the checkpoint must be inactivated to allow resumption of cell cycling and entry into mitosis. Though only beginning to be understood, here we review current data regarding checkpoint termination signals acting on Chk1 and its' upstream regulators.
authors.affiliation: Department of Oncological Sciences, Mount Sinai School of Medicine, New York, NY 10029, USA.
authors.forename: Teresa M
authors.initials: TM
authors.lastname: Calonge
authors.forename: Matthew J
authors.initials: MJ
authors.lastname: O'Connell
mesh_terms: D000071877:Checkpoint Kinase 1; D004249:DNA Damage / Q000502:physiology*; D016195:G2 Phase / Q000502:physiology*; D005786:Gene Expression Regulation / Q000502:physiology*; D018816:Genes, cdc / Q000502:physiology*; D010766:Phosphorylation; D011494:Protein Kinases / Q000235:genetics / Q000378:metabolism / Q000502:physiology*
chemical_list: D011494:Protein Kinases; C000605867:CHEK1 protein, human; D000071877:Checkpoint Kinase 1