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BRIT1 regulates early DNA damage response, chromosomal integrity, and cancer.

BRIT1, initially identified as an hTERT repressor, has additional functions at DNA damage checkpoints. Here, we demonstrate that BRIT1 formed nuclear foci minutes after irradiation. The foci of BRIT1 colocalized with 53BP1, MDC1, NBS1, ATM, RPA, and ATR. BRIT1 was required for activation of these elements, indicating that BRIT1 is a proximal factor in the DNA damage response pathway. Depletion of BRIT1 increased the accumulation of chromosomal aberrations. In addition, decreased levels of BRIT1 were detected in several types of human cancer, with BRIT1 expression being inversely correlated with genomic instability and metastasis. These results identify BRIT1 as a crucial DNA damage regulator in the ATM/ATR pathways and suggest that it functions as a tumor suppressor gene.

Pubmed ID: 16872911


  • Rai R
  • Dai H
  • Multani AS
  • Li K
  • Chin K
  • Gray J
  • Lahad JP
  • Liang J
  • Mills GB
  • Meric-Bernstam F
  • Lin SY


Cancer cell

Publication Data

August 14, 2006

Associated Grants

  • Agency: NCI NIH HHS, Id: P01 CA64602
  • Agency: NCI NIH HHS, Id: P50 CA83639
  • Agency: NCI NIH HHS, Id: R01 CA112291-01A1
  • Agency: NCI NIH HHS, Id: U54 CA112970
  • Agency: NCI NIH HHS, Id: U54 CA112970-02

Mesh Terms

  • Base Sequence
  • Breast Neoplasms
  • Cell Line, Tumor
  • Cell Nucleus
  • Cell Transformation, Neoplastic
  • Chromatin
  • Chromosome Aberrations
  • DNA Damage
  • Female
  • Gene Dosage
  • Humans
  • Molecular Sequence Data
  • Mutation
  • Nerve Tissue Proteins
  • Nuclear Proteins
  • Ovarian Neoplasms
  • Trans-Activators
  • Tumor Suppressor Proteins