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Kinases that control the cell cycle in response to DNA damage: Chk1, Chk2, and MK2

H Christian Reinhardt1, Michael B Yaffe

  • 1David H Koch Institute for Integrative Cancer Research, Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.

Current Opinion in Cell Biology
|February 24, 2009
PubMed

Insights

Eukaryotic cells activate cell cycle checkpoints to halt progression upon DNA damage, recruiting repair pathways. A third kinase pathway involving p38MAPK and MK2 has emerged alongside ATM/Chk2 and ATR/Chk1.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Genetics

Background:

  • Eukaryotic cells employ cell cycle checkpoints to respond to DNA damage.
  • These checkpoints involve complex kinase signaling networks that arrest cell cycle progression.
  • Checkpoint activation also facilitates DNA repair and, if necessary, cell elimination.

Purpose of the Study:

  • To review recent advancements in understanding the eukaryotic DNA damage response.
  • To highlight the roles of Chk1, Chk2, p38MAPK, and MK2 in DNA damage signaling.

Main Methods:

  • Review of existing literature on DNA damage response pathways.
  • Emphasis on kinase signaling networks including ATM/Chk2, ATR/Chk1, and p38MAPK/MK2.

Main Results:

  • The DNA damage response is traditionally divided into ATM/Chk2 (for double-strand breaks) and ATR/Chk1 (for single-strand breaks) pathways.
  • Both pathways converge on inhibiting Cdc25, a cell cycle regulator.
  • A third pathway, p38MAPK/MK2, activated downstream of ATM and ATR, has recently been identified.

Conclusions:

  • The p38MAPK/MK2 pathway represents a significant addition to the known DNA damage response effectors.
  • MK2 shares substrate homology with Chk1 and Chk2, suggesting functional overlap.
  • Further research into these kinase pathways is crucial for a comprehensive understanding of DNA damage management.

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