Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2001 Apr 5;20(15):1882-91.
doi: 10.1038/sj.onc.1204278.

The p107 tumor suppressor induces stable E2F DNA binding to repress target promoters

R J O'Connor  1 , J E Schaley, G Feeney, P Hearing
Affiliations

The p107 tumor suppressor induces stable E2F DNA binding to repress target promoters

R J O'Connor et al. Oncogene. .

Abstract

E2F transcription factors are key players in the regulation of proliferation, apoptosis, and differentiation in mammalian cells. E2Fs are negatively regulated by members of the retinoblastoma protein family, Rb, p107 and p130. During adenovirus infection, viral proteins are expressed that displace Rb family members from E2Fs and recruit E2F complexes to viral and cellular promoter regions. This recruitment of E2F involves the induction of stable E2F binding to inverted E2F binding sites in the Ad E2a and cellular E2F-1 promoters and induces both viral and cellular gene expression. The cellular p107 tumor suppressor also displays such regulation of E2F DNA binding activity. p107 induces stable E2F-4/DP binding to inverted E2F binding sites in the Ad E2a and cellular E2F-1 promoters. The induction of E2F DNA binding by p107 minimally requires the sequences in p107 that mediate E2F interaction. The related tumor suppressor, p130, also effects this function. p107 levels increase substantially as cells progress through S phase. p107 induction of E2F DNA binding was observed primarily in S phase cells coincident with the increase in p107 protein levels. The results of promoter activity assays directly correlate the induction of E2F DNA binding by p107 with effective transcriptional repression. These results support a model in which p107 and p130 induce the stable binding of E2F complexes to promoters that drive expression of critical regulatory proteins such as E2F-1. Since p107 and p130 bind histone deacetylase complexes (HDACs) which repress promoter activity, p107-E2F and p130-E2F would stably recruit repressor complexes to effect efficient promoter repression.

PubMed Disclaimer

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

Publication types

MeSH terms

LinkOut - more resources