Evidence map›Paper›PMID 11511545›Full record

ArticleGenes & development2001

Functional antagonism between E2F family members.

M V Frolov, D S Huen, O Stevaux, D Dimova, K Balczarek-Strang, M Elsdon, N J Dyson

Open access · diamondAbstract read
In one paragraph

Article in Genes & development, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers.

0numbers the graph read from it
0cells of the map it votes in
92citing papers in PubMed
–field-weighted citation impact
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

92 citing papers in PubMed, 168 citations in OpenAlex.

  1. Long noncoding RNAScience advances · 2024
    Article
  2. Article
  3. E2F regulation of theProceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  4. Article
  5. Article
  6. Regulation and coordination of the different DNA damage responses inFrontiers in cell and developmental biology · 2022
    Review
  7. Article
  8. The Krüppel-like factor Cabut has cell cycle regulatory properties similar to E2F1.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  9. Article
  10. Selective repression of the Drosophila cyclin B promoter by retinoblastoma and E2F proteins.Biochimica et biophysica acta. Gene regulatory mechanisms · 2020
    Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. The broken cycle: E2F dysfunction in cancer.Nature reviews. Cancer · 2019
    Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. TheBiology open · 2017
    Article

32 more citing papers are in PubMed but not listed here.

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

7 authors at 4 institutions in 2 countries.

M V FrolovMassachusetts General Hospital Cancer Center, Charlestown, Massachusetts 02129, USA.
D S Huen
O Stevaux
D Dimova
K Balczarek-Strang
M Elsdon
N J Dyson
Cancer Research UK · GBUniversity of Cambridge · GBHarvard University Press · USMassachusetts General Hospital · US

Funding

The E2F/RBF networkR01GM053203 · NIGMS · MASSACHUSETTS GENERAL HOSPITAL · PI DYSON, NICHOLAS J · 1995 to 2010
$4.2M
NIGMS NIH HHS GM53203NIGMS NIH HHS R01 GM053203
6 · The paper itself

Abstract

E2F is a heterogenous transcription factor and its role in cell cycle control results from the integrated activities of many different E2F family members. Unlike mammalian cells, that have a large number of E2F-related genes, the Drosophila genome encodes just two E2F genes, de2f1 and de2f2. Here we show that de2f1 and de2f2 provide different elements of E2F regulation and that they have opposing functions during Drosophila development. dE2F1 and dE2F2 both heterodimerize with dDP and bind to the promoters of E2F-regulated genes in vivo. dE2F1 is a potent activator of transcription, and the loss of de2f1 results in the reduced expression of E2F-regulated genes. In contrast, dE2F2 represses the transcription of E2F reporters and the loss of de2f2 function results in increased and expanded patterns of gene expression. The loss of de2f1 function has previously been reported to compromise cell proliferation. de2f1 mutant embryos have reduced expression of E2F-regulated genes, low levels of DNA synthesis, and hatch to give slow-growing larvae. We find that these defects are due in large part to the unchecked activity of dE2F2, since they can be suppressed by mutation of de2f2. Examination of eye discs from de2f1; de2f2 double-mutant animals reveals that relatively normal patterns of DNA synthesis can occur in the absence of both E2F proteins. This study shows how repressor and activator E2Fs are used to pattern transcription and how the net effect of E2F on cell proliferation results from the interplay between two types of E2F complexes that have antagonistic functions.

Indexed as

Cell Cycle ProteinsDNA-Binding ProteinsDrosophila ProteinsAllelesAnimalsAnimals, Genetically ModifiedCell CycleDrosophilaE2F2 Transcription FactorE2F Transcription FactorsEyeGene DeletionGene Expression RegulationPhenotypeRetinoblastoma ProteinTranscription FactorsCell Cycle ProteinsDNA-Binding ProteinsDrosophila ProteinsE2F2 Transcription FactorE2F Transcription FactorsRbf protein, DrosophilaRetinoblastoma ProteinTranscription Factors

Identifiers

PMID11511545
PMCPMC312757
OpenAlexW2082400881

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.