Oswald, F and Dobner, T and Lipp, M (1996) The E2F transcription factor activates a replication-dependent human H2A gene in early S phase of the cell cycle. MOLECULAR AND CELLULAR BIOLOGY, 16 (5). pp. 1889-1895. ISSN 0270-7306,
Full text not available from this repository.Abstract
Histone gene expression is restricted to the S phase of the cell cycle, control is mediated by a complex network of sequence-specific DNA-binding factors and protein-protein interactions in response to cell cycle progression, To further Investigate the regulatory functions that are associated at the transcriptional level, we analyzed the regulation of a replication-dependent human H2A.1-H2B.2 gene pair. We found that transcription factor E2F binds specifically to an E2F recognition motif in the H2A.1 promoter region. Activation of the H2A.1 promoter by E2F-1 was shown by use of luciferase reporter constructs of the intergenic promoter region. Overexpression of the human retinoblastoma suppressor gene product RE suppressed E2F-1 mediated transcriptional activation, indicating an E2F-dependent regulation of promoter activity during the G(1)-to-S-phase transition, Furthermore, the activity of the H2A.1 promoter was also downregulated by overexpression of the RE-related p107, a protein that has been detected In S-phase-specific protein complexes of cyclin A, E2F, and cdk2, In synchronized HeLa cells, expression of luciferase activity was synthesis and was dependent on the presence of an E2F-binding site in the H2A.1 promoter, Together with the finding that E2F-binding motifs are highly conserved in H2A promoters of other species, our results suggest that E2F plays an important role in the coordinate regulation of S-phase-specific histone gene expression.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | DNA-BINDING ACTIVITY; CONSENSUS ELEMENT; TRANS-ACTIVATION; PROTEIN; EXPRESSION; PROMOTER; PRODUCT; RB; IDENTIFICATION; SEQUENCES; |
| Depositing User: | Dr. Gernot Deinzer |
| Last Modified: | 19 Oct 2022 08:35 |
| URI: | https://pred.uni-regensburg.de/id/eprint/51750 |
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