Evidence map›Paper›PMID 7933066›Full record

ArticleJournal of virology1994

Mutually exclusive interaction of the adenovirus E4-6/7 protein and the retinoblastoma gene product with internal domains of E2F-1 and DP-1.

R J O'Connor, P Hearing

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.1field-weighted citation impact, top 13% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

16 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Metabolic Control by DNA Tumor Virus-Encoded Proteins.Pathogens (Basel, Switzerland) · 2021
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Crystal structure of the retinoblastoma tumor suppressor protein bound to E2F and the molecular basis of its regulation.Proceedings of the National Academy of Sciences of the United States of America · 2003
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Adenovirus E4orf6 oncoprotein modulates the function of the p53-related protein, p73.Proceedings of the National Academy of Sciences of the United States of America · 1998
    Article
  13. Article
  14. Article
  15. Article
  16. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

R J O'ConnorDepartment of Molecular Genetics and Microbiology, State University of New York, Stony Brook 11794.
P Hearing
Stony Brook University · US

Funding

TUMOR VIRUS-HOST INTERACTIONSP01CA028146 · NCI · STATE UNIVERSITY NEW YORK STONY BROOK · PI HEARING, PATRICK · 1986 to 2005
$9.9M
VIRAL ONCOLOGYT32CA009176 · NCI · STATE UNIVERSITY NEW YORK STONY BROOK · PI HEARING, PATRICK · 1985 to 2012
$5.2M
NCI NIH HHS CA09176NCI NIH HHS CA28146
6 · The paper itself

Abstract

The binding of E2F to the adenovirus (Ad) E2a promoter is stimulated by the Ad E4-6/7 protein. E2F DNA binding activity is composed of a heterodimer of related but distinct proteins of the E2F-1 and DP-1 families. The E4-6/7 protein induces the cooperative and stable binding of E2F to an inverted repeat binding site in the E2a promoter apparently by providing a dimerization interface to two adjacent E2F heterodimers. The product of the retinoblastoma gene product (Rb) represses the transcriptional activity of E2F by direct protein-protein interaction. In this report, we have examined the regions of E2F-1 and DP-1 that are required for the induction of cooperative E2F binding to the E2a promoter by the E4-6/7 protein. Our results demonstrate that an internal segment of E2F-1, that is conserved among members of the E2F family, is required for functional interaction with the E4-6/7 product. Consistent with this observation, other members of the E2F family (E2F-2 and E2F-3) productively interact with E4-6/7. DP-1 also is necessary for stable interaction with E4-6/7 and an internal segment of DP-1 is required that is positioned in a location similar to that of the conserved E2F-1 domain. Interestingly, the binding of E4-6/7 and the binding of Rb to E2F are mutually exclusive, and our results show that the same internal segments of E2F-1 and DP-1 that are required for E4-6/7 binding are also required for stable interaction with Rb. These results suggest that the Ad E4-6/7 protein mimics Rb in part for the protein interaction requirements for E2F binding, although with different functional consequences. While Rb binding represses E2F activity, the E4-6/7 protein stimulates transactivation of the Ad E2a promoter.

Indexed as

Carrier ProteinsCell Cycle ProteinsDNA-Binding ProteinsAdenoviridaeAdenovirus E4 ProteinsBase SequenceDNAE2F1 Transcription FactorE2F3 Transcription FactorE2F Transcription FactorsMolecular Sequence DataPromoter Regions, GeneticRetinoblastoma-Binding Protein 1Retinoblastoma ProteinTranscription FactorsAdenovirus E4 ProteinsCarrier ProteinsCell Cycle ProteinsDNADNA-Binding ProteinsE2F1 Transcription FactorE2F3 Transcription FactorE2F Transcription FactorsRetinoblastoma-Binding Protein 1Retinoblastoma ProteinTranscription Factors

Identifiers

PMID7933066
PMCPMC237120
OpenAlexW2163981883

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.