| First Author | Contreras AU | Year | 2013 |
| Journal | J Cell Biol | Volume | 201 |
| Issue | 3 | Pages | 427-37 |
| PubMed ID | 23629966 | Mgi Jnum | J:197027 |
| Mgi Id | MGI:5490676 | Doi | 10.1083/jcb.201205064 |
| Citation | Contreras AU, et al. (2013) Deacetylation of p53 induces autophagy by suppressing Bmf expression. J Cell Biol 201(3):427-37 |
| abstractText | Interferon gamma (IFN-gamma)-induced cell death is mediated by the BH3-only domain protein, Bik, in a p53-independent manner. However, the effect of IFN-gamma on p53 and how this affects autophagy have not been reported. The present study demonstrates that IFN-gamma down-regulated expression of the BH3 domain-only protein, Bmf, in human and mouse airway epithelial cells in a p53-dependent manner. p53 also suppressed Bmf expression in response to other cell death-stimulating agents, including ultraviolet radiation and histone deacetylase inhibitors. IFN-gamma did not affect Bmf messenger RNA half-life but increased nuclear p53 levels and the interaction of p53 with the Bmf promoter. IFN-gamma-induced interaction of HDAC1 and p53 resulted in the deacetylation of p53 and suppression of Bmf expression independent of p53's proline-rich domain. Suppression of Bmf facilitated IFN-gamma-induced autophagy by reducing the interaction of Beclin-1 and Bcl-2. Furthermore, autophagy was prominent in cultured bmf(-/-) but not in bmf(+/+) cells. Collectively, these observations show that deacetylation of p53 suppresses Bmf expression and facilitates autophagy. |
