Turning off the G2 DNA damage checkpoint

Teresa M. Calonge, Matthew J. O'Connell

Research output: Contribution to journalReview articlepeer-review

31 Scopus citations


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.

Original languageEnglish
Pages (from-to)136-140
Number of pages5
JournalDNA Repair
Issue number2
StatePublished - 1 Feb 2008


  • Checkpoint
  • Chk1
  • Protein kinase
  • Protein phosphatase
  • Ubiquitin-dependent proteolysis


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