| First Author | Sax JK | Year | 2002 |
| Journal | Nat Cell Biol | Volume | 4 |
| Issue | 11 | Pages | 842-9 |
| PubMed ID | 12402042 | Mgi Jnum | J:80564 |
| Mgi Id | MGI:2446357 | Doi | 10.1038/ncb866 |
| Citation | Sax JK, et al. (2002) BID regulation by p53 contributes to chemosensitivity. Nat Cell Biol 4(11):842-9 |
| abstractText | The role of the p53 protein (encoded by TP53) in tumour suppression relies partly on the ability of p53 to regulate the transcription of genes that are important in cell-cycle arrest and in apoptosis. But the apoptotic pathway mediated by p53 is not fully understood. Here we show that BID, a member of the pro-apoptotic Bcl-2 family of proteins, is regulated by p53. BID mRNA is increased in a p53-dependent manner in vitro and in vivo, with strong expression in the splenic red pulp and colonic epithelium of gamma-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. |
