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Papers In Press, published online ahead of print January 3, 2002
Department of Radiation Oncology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213
Corresponding Author: Qzhan{at}pitt.edu
SUMMARY BRCA1, a breast and ovarian cancer susceptibility gene, has been implicated in gene regulation. Previous studies demonstrate that BRCA1 induces GADD45, a p53-regulated and stress-inducible gene that plays an important role in cellular response to DNA damage. However, the mechanism(s) by which BRCA1 regulates GADD45 remains unclear. In this report, we have shown that BRCA1 activation of the GADD45 promoter is mediated through the OCT-1 and CAAT motifs located at the GADD45 promoter region. Site-directed mutations of both OCT-1 and CAAT motifs abrogate induction of the GADD45 promoter by BRCA1. Both OCT-1 and CAAT motifs are able to confer BRCA1 inducibility in a non-related minimal promoter. Physical associations of BRCA1 protein with transcription factors Oct-1 and NF-YA, which directly bind to the OCT-1 and CAAT motifs, are established by biotin-streptavidin pull-down and coimmunoprecipitation assays. Such protein interactions are required for interaction of BRCA1 with the GADD45 promoter since either immunodepletion of Oct-1 and NF-YA proteins or mutations in the OCT1and CAAT motifs disrupt BRCA1 binding to the GADD45 promoter. These findings indicate that BRCA1 can upregulate its targeted genes through protein-protein interactions and provide a novel mechanism by which BRCA1 participates in transcriptional regulation.
J. Biol. Chem, 10.1074/jbc.M110225200
Submitted on October 24, 2001
Revised on December 18, 2001
Accepted on January 3, 2002
BRCA1 regulates GADD45 through its interactions with the OCT-1 and CAAT motifs
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