Joanna K. Sax1, Peiwen Fei1, Maureen E. Murphy2, Eric Bernhard3, Stanley J. Korsmeyer4
& Wafik S. El-Deiry11
Laboratory of Molecular Oncology and Cell Cycle Regulation, Howard Hughes Medical Institute, Departments of Medicine, Pharmacology, and Genetics, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA
2
Department of Pharmacology, Fox Chase Cancer Center, Philadelphia, PA 19111, USA
3
Department of Radiation Oncology, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA
4
Howard Hughes Medical Institute, Departments of Pathology and Medicine, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
Correspondence should be addressed to Wafik S. El-Deiry wafik@mail.med.upenn.edu
-irradiated mice. Both the human and the mouse BID genomic loci contain p53-binding DNA response elements that bind p53 and mediate p53-dependent transactivation of a reporter gene. In addition, BID-null mouse embryonic fibroblasts are more resistant than are wild-type fibroblasts to the DNA damaging agent adriamycin and the nucleotide analogue 5-fluorouracil, both of which stabilize endogenous p53. Our results indicate that BID is a p53-responsive 'chemosensitivity gene' that may enhance the cell death response to chemotherapy.
