Functional interplay between ATM/ATR-mediated DNA damage response and DNA repair pathways in oxidative stress

Cell Mol Life Sci. 2014 Oct;71(20):3951-67. doi: 10.1007/s00018-014-1666-4. Epub 2014 Jun 20.

Abstract

To maintain genome stability, cells have evolved various DNA repair pathways to deal with oxidative DNA damage. DNA damage response (DDR) pathways, including ATM-Chk2 and ATR-Chk1 checkpoints, are also activated in oxidative stress to coordinate DNA repair, cell cycle progression, transcription, apoptosis, and senescence. Several studies demonstrate that DDR pathways can regulate DNA repair pathways. On the other hand, accumulating evidence suggests that DNA repair pathways may modulate DDR pathway activation as well. In this review, we summarize our current understanding of how various DNA repair and DDR pathways are activated in response to oxidative DNA damage primarily from studies in eukaryotes. In particular, we analyze the functional interplay between DNA repair and DDR pathways in oxidative stress. A better understanding of cellular response to oxidative stress may provide novel avenues of treating human diseases, such as cancer and neurodegenerative disorders.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Ataxia Telangiectasia Mutated Proteins / metabolism*
  • Checkpoint Kinase 1
  • Checkpoint Kinase 2 / metabolism
  • DNA Damage
  • DNA Repair / physiology*
  • DNA-Binding Proteins / metabolism
  • Humans
  • Oxidative Stress / physiology*
  • Protein Kinases / metabolism
  • Signal Transduction

Substances

  • DNA-Binding Proteins
  • Protein Kinases
  • Checkpoint Kinase 2
  • ATR protein, human
  • Ataxia Telangiectasia Mutated Proteins
  • CHEK1 protein, human
  • Checkpoint Kinase 1