Display Settings:

Format

Send to:

Choose Destination
See comment in PubMed Commons below
Cancer Lett. 2012 Dec 31;327(1-2):103-10. doi: 10.1016/j.canlet.2011.12.004. Epub 2011 Dec 9.

New insights into the roles of ATM and DNA-PKcs in the cellular response to oxidative stress.

Author information

  • 1Department of Radiation Oncology/Division of Molecular Radiation Biology, University of Texas Southwestern Medical Center at Dallas, 75390-9187, USA. benjamin.chen@utsouthwestern.edu

Abstract

Reactive oxygen species (ROS) are induced by a variety of endogenous and exogenous sources. At pathologically high levels, ROS cause damage to biological molecules, including DNA. The damage sustained by DNA likely plays a key role in the pathogenesis of aging and carcinogenesis. Extensive research has established in detail the mechanism of cellular response to oxidative stress. Attention is now focused on identifying the molecular contributions of the key DNA damage response kinases ataxia telangiectasia mutated (ATM), DNA-dependent protein kinase catalytic subunit (DNA-PKcs), and ATM- and Rad3-related (ATR) in the oxidative stress response. In this review, we will provide an update of the current evidence regarding the involvement of these related DNA damage response kinases in oxidative DNA lesion repair and signaling responses. The growing understanding of the involvement of ATM, DNA-PKcs, and ATR in the oxidative stress response will offer new possibilities for the treatment of ROS-related diseases.

Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.

PMID:
22155347
[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Icon for Elsevier Science
    Loading ...
    Write to the Help Desk