BRCA1 Augments Transcription by the NF-κB Transcription Factor by Binding to the Rel Domain of the p65/RelA Subunit

• DOI: 10.1074/jbc.m303076200
• Publication Date: 2003-07-12T13:05:42Z
• Authors: Miriam Benezra; Nathalie Chevallier; Debra J. Morrison; Timothy K. MacLac...; Wafik S. El-Deiry; Jonathan D. Licht
• Keywords: Transcription; TAF2; General transcription factor

BRCA1 is a tumor suppressor gene mutated in cases of hereditary breast and ovarian cancer. protein involved apoptosis growth/tumor suppression. In this study, we present evidence that p65/RelA, one the two subunits transcription factor NF-kappaB, binds to protein. Treatment 293T cells with cytokine necrosis factor-alpha induces an interaction between endogenous p65/RelA BRCA1. GST-protein affinity assay experiments reveal Rel homology domain subunit NF-kappaB interacts multiple sites within N-terminal region Transient transfection significantly enhances ability or interleukin-1beta activate from promoters target genes. Mutation NF-kappaB-binding reporter blocks effect on transcription. Also genes inhibited by super-stable inhibitor chemical SN-50. These data indicate acts as co-activator NF-kappaB. addition, show infected adenovirus expressing up-regulate expression Fas interferon-beta. Together, information suggests may play role cell life-death decisions following stress modulation activity