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Papers In Press, published online ahead of print May 30, 2001
J. Biol. Chem, 10.1074/jbc.C100265200
Submitted on May 22, 2001
Revised on May 30, 2001
Accepted on May 30, 2001
Center for Cancer Research, National Cancer Institute, Gaithersburg, MD 20877
Corresponding Author: Apreliko{at}mail.nih.gov
BRCA1 gene is a tumor suppressor for breast and ovarian cancers with the putative role in DNA repair and transcription. To characterize the role of BRCA1 in transcriptional regulation, we analyzed gene expression profiles of mouse embryonic stem (ES) cells deficient in BRCA1 using microarray technology. We found that loss of BRCA1 correlated with decreased expression of several groups of genes including stress response genes, cytoskeleton genes and genes involved in protein synthesis and degradation. Previous study showed that BRCA1 is a transcriptional co-activator of p53 protein, however the majority of p53 target genes remained at the same expression levels in BRCA1 knock out cells as in the wild type cells. The only p53 target gene downregulated with the loss of BRCA1 was 14-3-3s, a major G2/M checkpoint control gene. Similar to cells with decreased 14-3-3s activity, BRCA1 deficient cells were unable to sustain G2/M growth arrest after exposure to ionizing radiation. We find that BRCA1 induction of 14-3-3s requires the presence of wild type p53, and can be regulated by a minimal p53 response element.
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