| First Author | Vaughan PS | Year | 1998 |
| Journal | J Biol Chem | Volume | 273 |
| Issue | 1 | Pages | 194-9 |
| PubMed ID | 9417064 | Mgi Jnum | J:45041 |
| Mgi Id | MGI:1101655 | Doi | 10.1074/jbc.273.1.194 |
| Citation | Vaughan PS, et al. (1998) Cell cycle regulation of histone H4 gene transcription requires the oncogenic factor IRF-2. J Biol Chem 273(1):194-9 |
| abstractText | Histone genes display a peak in transcription in early S phase and are ideal models for cell cycle-regulated gene expression. We have previously shown that the transcription factor interferon regulatory factor 2 (IRF-2) can activate histone H4 gene expression. In this report we establish that a mouse histone H4 gene and its human homolog lose stringent cell cycle control in synchronized embryonic fibroblasts in which IRF-2 has been ablated. We also show that there are reduced mRNA levels of this endogenous mouse histone H4 gene in the IRF-2(-/-) cells. Strikingly, the overall mRNA level and cell cycle regulation of histone H4 transcription are restored when IRF-2 is reintroduced to these cells. IRF-2 is a negative regulator of the interferon response and has oncogenic potential, but little is known of the mechanism of these activities. Our results suggest that IRF-2 is an active player in E2F-independent cell cycle-regulated gene expression at the G1/S phase transition. IRF-2 was previously considered a passive antagonist to the tumor suppressor IRF-1 but can now join other oncogenic factors such as c-Myb and E2F1 that are predicted to mediate their transforming capabilities by actively regulating genes necessary for cell cycle progression. |
