Evidence map›Paper›PMID 24662053›Full record

ArticleMolecular and cellular biology2014

A retinoblastoma allele that is mutated at its common E2F interaction site inhibits cell proliferation in gene-targeted mice.

Matthew J Cecchini, Michael J Thwaites, Srikanth Talluri, James I MacDonald, Daniel T Passos, Jean-Leon Chong, Paul Cantalupo, Paul M Stafford, M Teresa Sáenz-Robles, Sarah M Francis and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

24 citing papers in PubMed, 36 citations in OpenAlex.

  1. Chromatin association promotes UBR5-mediated degradation of Rb.bioRxiv : the preprint server for biology · 2026
    Article
  2. Article
  3. Review
  4. Article
  5. Monitoring the Cell Cycle of Tumor Cells in Mouse Models of Human Cancer.Cold Spring Harbor perspectives in medicine · 2023
    Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Molecular and cellular biology · 2019
    Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Conservation and divergence of C-terminal domain structure in the retinoblastoma protein family.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  17. Targeting nuclear thymidylate biosynthesis.Molecular aspects of medicine · 2017
    Review
  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

14 authors at 3 institutions in 4 countries.

Matthew J CecchiniLondon Regional Cancer Program, Western University, London, Ontario, Canada.
Michael J Thwaites
Srikanth Talluri
James I MacDonald
Daniel T Passos
Jean-Leon Chong
Paul Cantalupo
Paul M Stafford
M Teresa Sáenz-Robles
Sarah M Francis
James M Pipas
Gustavo Leone
Ian Welch
Frederick A Dick
Western University · CAUniversity of Pittsburgh · USCancer Genetics (United States) · US

Funding

Translational Therapeutics Research Program (TT)P30CA016058 · NCI · OHIO STATE UNIVERSITY · PI Jennifer A. Woyach · 1985 to 2026
$132.3M
Suppression of Mammary Tumorigenesis by Stromal p53P01CA097189 · NCI · OHIO STATE UNIVERSITY · PI ROSOL, THOMAS J · 2004 to 2016
$16.1M
Expression of Simian Virus 40 T antigens in IntestineR01CA098956 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI PIPAS, JAMES M · 2003 to 2013
$3.2M
CIHR MOP-89765NCI NIH HHS P01 CA097189NCI NIH HHS P30 CA016058NCI NIH HHS R01 CA098956NCI NIH HHS R01 CA98956
6 · The paper itself

Abstract

The retinoblastoma protein (pRB) is best known for regulating cell proliferation through E2F transcription factors. In this report, we investigate the properties of a targeted mutation that disrupts pRB interactions with the transactivation domain of E2Fs. Mice that carry this mutation endogenously (Rb1(ΔG)) are defective for pRB-dependent repression of E2F target genes. Except for an accelerated entry into S phase in response to serum stimulation, cell cycle regulation in Rb1(ΔG/ΔG) mouse embryonic fibroblasts (MEFs) strongly resembles that of the wild type. In a serum deprivation-induced cell cycle exit, Rb1(ΔG/ΔG) MEFs display a magnitude of E2F target gene derepression similar to that of Rb1(-/-) cells, even though Rb1(ΔG/ΔG) cells exit the cell cycle normally. Interestingly, cell cycle arrest in Rb1(ΔG/ΔG) MEFs is responsive to p16 expression and gamma irradiation, indicating that alternate mechanisms can be activated in G1 to arrest proliferation. Some Rb1(ΔG/ΔG) mice die neonatally with a muscle degeneration phenotype, while the others live a normal life span with no evidence of spontaneous tumor formation. Most tissues appear histologically normal while being accompanied by derepression of pRB-regulated E2F targets. This suggests that non-E2F-, pRB-dependent pathways may have a more relevant role in proliferative control than previously identified.

Indexed as

AdenocarcinomaAllelesAnimalsBinding SitesCell LineCell ProliferationCyclin-Dependent Kinase Inhibitor p16E2F Transcription FactorsFibroblastsGene TargetingMiceMice, KnockoutMutationPituitary NeoplasmsRetinoblastoma ProteinS PhaseCyclin-Dependent Kinase Inhibitor p16E2F Transcription FactorsRetinoblastoma Protein

Identifiers

PMID24662053
PMCPMC4019062
OpenAlexW2158106167

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.