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Chromatin association of rad17 is required for an ataxia telangiectasia and rad-related kinase-mediated S-phase checkpoint in response to low-dose ultraviolet radiation.

Publication ,  Journal Article
Garg, R; Callens, S; Lim, D-S; Canman, CE; Kastan, MB; Xu, B
Published in: Mol Cancer Res
June 2004

Activation of the S-phase checkpoint results in an inhibition of DNA synthesis in response to DNA damage. This is an active cellular response that may enhance cell survival and limit heritable genetic abnormalities. While much attention has been paid to elucidating signal transduction pathways regulating the ionizing radiation-induced S-phase checkpoint, less is known about whether UV radiation initiates the process and the mechanism controlling it. Here, we demonstrate that low-dose UV radiation activates an S-phase checkpoint that requires the ataxia telangiectasia and Rad-related kinase (ATR). ATR regulates the S-phase checkpoint through phosphorylation of the downstream target structural maintenance of chromosomal protein 1. Furthermore, the ATPase activity of Rad17 is crucial for its chromatin association and for the functional effects of ATR activation in response to low-dose UV radiation. These results suggest that low-dose UV radiation activates an S-phase checkpoint requiring ATR-mediated signal transduction pathway.

Duke Scholars

Published In

Mol Cancer Res

ISSN

1541-7786

Publication Date

June 2004

Volume

2

Issue

6

Start / End Page

362 / 369

Location

United States

Related Subject Headings

  • Ultraviolet Rays
  • S Phase
  • Protein Serine-Threonine Kinases
  • Protein Binding
  • Phosphorylation
  • Oncology & Carcinogenesis
  • Mutation
  • Humans
  • Developmental Biology
  • DNA-Binding Proteins
 

Citation

APA
Chicago
ICMJE
MLA
NLM

Published In

Mol Cancer Res

ISSN

1541-7786

Publication Date

June 2004

Volume

2

Issue

6

Start / End Page

362 / 369

Location

United States

Related Subject Headings

  • Ultraviolet Rays
  • S Phase
  • Protein Serine-Threonine Kinases
  • Protein Binding
  • Phosphorylation
  • Oncology & Carcinogenesis
  • Mutation
  • Humans
  • Developmental Biology
  • DNA-Binding Proteins