• Register
X
Forgot Password

If you have forgotten your password you can enter your email here and get a temporary password sent to your email.

X

Leaving Community

Are you sure you want to leave this community? Leaving the community will revoke any permissions you have been granted in this community.

No
Yes

Radiation-induced assembly of Rad51 and Rad52 recombination complex requires ATM and c-Abl.

Cells from individuals with the recessive cancer-prone disorder ataxia telangiectasia (A-T) are hypersensitive to ionizing radiation (I-R). ATM (mutated in A-T) is a protein kinase whose activity is stimulated by I-R. c-Abl, a nonreceptor tyrosine kinase, interacts with ATM and is activated by ATM following I-R. Rad51 is a homologue of bacterial RecA protein required for DNA recombination and repair. Here we demonstrate that there is an I-R-induced Rad51 tyrosine phosphorylation, and this induction is dependent on both ATM and c-Abl. ATM, c-Abl, and Rad51 can be co-immunoprecipitated from cell extracts. Consistent with the physical interaction, c-Abl phosphorylates Rad51 in vitro and in vivo. In assays using purified components, phosphorylation of Rad51 by c-Abl enhances complex formation between Rad51 and Rad52, which cooperates with Rad51 in recombination and repair. After I-R, an increase in association between Rad51 and Rad52 occurs in wild-type cells but not in cells with mutations that compromise ATM or c-Abl. Our data suggest signaling mediated through ATM, and c-Abl is required for the correct post-translational modification of Rad51, which is critical for the assembly of Rad51 repair protein complex following I-R.

Pubmed ID: 10212258

Authors

  • Chen G
  • Yuan SS
  • Liu W
  • Xu Y
  • Trujillo K
  • Song B
  • Cong F
  • Goff SP
  • Wu Y
  • Arlinghaus R
  • Baltimore D
  • Gasser PJ
  • Park MS
  • Sung P
  • Lee EY

Journal

The Journal of biological chemistry

Publication Data

April 30, 1999

Associated Grants

  • Agency: NINDS NIH HHS, Id: 1RO1NS378381-01

Mesh Terms

  • Ataxia Telangiectasia Mutated Proteins
  • Cell Cycle Proteins
  • Checkpoint Kinase 2
  • DNA-Binding Proteins
  • Phosphorylation
  • Protein Binding
  • Protein Kinases
  • Protein Processing, Post-Translational
  • Protein-Serine-Threonine Kinases
  • Proteins
  • Proto-Oncogene Proteins c-abl
  • Rad51 Recombinase
  • Rad52 DNA Repair and Recombination Protein
  • Recombination, Genetic
  • Saccharomyces cerevisiae Proteins
  • Tumor Suppressor Proteins
  • Tyrosine