| First Author | Li Z | Year | 2010 |
| Journal | Oncogene | Volume | 29 |
| Issue | 18 | Pages | 2659-71 |
| PubMed ID | 20154723 | Mgi Jnum | J:160788 |
| Mgi Id | MGI:4455105 | Doi | 10.1038/onc.2010.19 |
| Citation | Li Z, et al. (2010) An HDAC1-binding domain within FATS bridges p21 turnover to radiation-induced tumorigenesis. Oncogene 29(18):2659-71 |
| abstractText | There is a gap between the initial formation of cells carrying radiation-induced genetic damage and their contribution to cancer development. Herein, we reveal a previously uncharacterized gene FATS through a genome-wide approach and demonstrate its essential role in regulating the abundance of p21 in surveillance of genome integrity. A large exon coding the NH2-terminal domain of FATS, deleted in spontaneous mouse lymphomas, is much more frequently deleted in radiation-induced mouse lymphomas. Its human counterpart is a fragile site gene at a previously identified loss of heterozygosity site. FATS is essential for maintaining steady-state level of p21 protein and sustaining DNA damage checkpoint. Furthermore, the NH2-terminal FATS physically interacts with histone deacetylase 1 (HDAC1) to enhance the acetylation of endogenous p21, leading to the stabilization of p21. Our results reveal a molecular linkage between p21 abundance and radiation-induced carcinogenesis. |
