Evidence map›Paper›PMID 21185283›Full record

ArticleDevelopmental biology2011

Cell proliferation in the absence of E2F1-3.

Pamela L Wenzel, Jean-Leon Chong, M Teresa Sáenz-Robles, Antoney Ferrey, John P Hagan, Yorman M Gomez, Ravi Rajmohan, Nidhi Sharma, Hui-Zi Chen, James M Pipas and 2 more

Abstract read
In one paragraph

Article in Developmental biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 2 pooled it
1.4field-weighted citation impact, top 19% 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

36 citing papers in PubMed, 2 syntheses or guidelines pooled it, 66 citations in OpenAlex.

  1. A comprehensive investigation of identifying miRNA biomarkers and their potential role in age-related cataract by meta-analysis and bioinformatics analysis.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2025
    Pooled it
  2. Pooled it
  3. Review
  4. Article
  5. Article
  6. Monitoring the Cell Cycle of Tumor Cells in Mouse Models of Human Cancer.Cold Spring Harbor perspectives in medicine · 2023
    Article
  7. Article
  8. Article
  9. Review
  10. CCBE1 in Cardiac Development and Disease.Frontiers in genetics · 2022
    Review
  11. Article
  12. Article
  13. Review
  14. The broken cycle: E2F dysfunction in cancer.Nature reviews. Cancer · 2019
    Review
  15. Article
  16. Critical Roles of E2F3 in Growth and Musculo-skeletal Phenotype in Mice.International journal of medical sciences · 2019
    Article
  17. Article
  18. Article
  19. Article
  20. 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

12 authors at 3 institutions in 1 country.

Pamela L WenzelDepartment of Molecular Virology, Immunology and Medical Genetics, Comprehensive Cancer Center, College of Medicine, The Ohio State University, Columbus, OH 43210, USA.
Jean-Leon Chong
M Teresa Sáenz-Robles
Antoney Ferrey
John P Hagan
Yorman M Gomez
Ravi Rajmohan
Nidhi Sharma
Hui-Zi Chen
James M Pipas
Michael L Robinson
Gustavo Leone
The Ohio State University · USMiami University · USUniversity of Pittsburgh · US

Funding

Suppression of Mammary Tumorigenesis by Stromal p53P01CA097189 · NCI · OHIO STATE UNIVERSITY · PI FERNANDEZ, SOLEDAD A · 2004 to 2016
$16.1M
THE ROLE OF FGF RECPETORS IN LENS DEVELOPMENTR01EY012995 · NEI · RESEARCH INST NATIONWIDE CHILDREN'S HOSP · PI ROBINSON, MICHAEL L · 2000 to 2018
$4.9M
Postdoctoral Training in Cancer GeneticsT32CA106196 · NCI · OHIO STATE UNIVERSITY · PI DE LA CHAPELLE, ALBERT · 2004 to 2013
$3.6M
E2F3 and embryonic developmentR01HD047470 · NICHD · OHIO STATE UNIVERSITY · PI LEONE, GUSTAVO WALTER · 2004 to 2008
$1.6M
E2F3 GENE LOCUS IN THE CONTROL OF CELL PROLIFERATIONR01CA085619 · NCI · OHIO STATE UNIVERSITY · PI LEONE, GUSTAVO WALTER · 2001 to 2005
$1.4M
E2F AND THE CONTROL OF APOPTOSISR01CA082259 · NCI · OHIO STATE UNIVERSITY · PI LEONE, GUSTAVO WALTER · 1999 to 2003
$840k
NCI NIH HHS 5 T32 CA106196-04NCI NIH HHS P01 CA097189NCI NIH HHS P01CA097189NCI NIH HHS R01 CA082259NCI NIH HHS R01 CA085619NCI NIH HHS R01CA82259NCI NIH HHS R01CA85619NCI NIH HHS T32 CA106196NEI NIH HHS R01 EY012995NEI NIH HHS R01EY012995NICHD NIH HHS R01 HD047470NICHD NIH HHS R01HD047470
6 · The paper itself

Abstract

E2F transcription factors regulate the progression of the cell cycle by repression or transactivation of genes that encode cyclins, cyclin dependent kinases, checkpoint regulators, and replication proteins. Although some E2F functions are independent of the Retinoblastoma tumor suppressor (Rb) and related family members, p107 and p130, much of E2F-mediated repression of S phase entry is dependent upon Rb. We previously showed in cultured mouse embryonic fibroblasts that concomitant loss of three E2F activators with overlapping functions (E2F1, E2F2, and E2F3) triggered the p53-p21(Cip1) response and caused cell cycle arrest. Here we report on a dramatic difference in the requirement for E2F during development and in cultured cells by showing that cell cycle entry occurs normally in E2f1-3 triply-deficient epithelial stem cells and progenitors of the developing lens. Sixteen days after birth, however, massive apoptosis in differentiating epithelium leads to a collapse of the entire eye. Prior to this collapse, we find that expression of cell cycle-regulated genes in E2F-deficient lenses is aberrantly high. In a second set of experiments, we demonstrate that E2F3 ablation alone does not cause abnormalities in lens development but rescues phenotypic defects caused by loss of Rb, a binding partner of E2F known to recruit histone deacetylases, SWI/SNF and CtBP-polycomb complexes, methyltransferases, and other co-repressors to gene promoters. Together, these data implicate E2F1-3 in mediating transcriptional repression by Rb during cell cycle exit and point to a critical role for their repressive functions in cell survival.

Indexed as

Cell ProliferationAnimalsApoptosisCell SurvivalDNA Breaks, Double-StrandedE2F1 Transcription FactorE2F2 Transcription FactorE2F3 Transcription FactorEpithelial CellsMiceMice, Inbred C57BLMice, KnockoutRepressor ProteinsRetinoblastoma ProteinTumor Suppressor Protein p53E2f1 protein, mouseE2F1 Transcription FactorE2f2 protein, mouseE2F2 Transcription FactorE2f3 protein, mouseE2F3 Transcription FactorRepressor ProteinsRetinoblastoma ProteinTumor Suppressor Protein p53

Identifiers

PMID21185283
PMCPMC3868453
OpenAlexW2047701672

What OpenQuestion holds

Textmetadata
LicenceTDM
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.