Evidence map›Paper›PMID 17072340›Full record

ArticleOncogene2007

Targeting an E2F site in the mouse genome prevents promoter silencing in quiescent and post-mitotic cells.

F Tavner, J Frampton, R J Watson

Abstract read
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In one paragraph

Article in Oncogene, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
0.5field-weighted citation impact, top 36% 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

26 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. Article
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  4. E2F regulation of theProceedings of the National Academy of Sciences of the United States of America · 2023
    Article
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  14. A CRISPR Path to Engineering New Genetic Mouse Models for Cardiovascular Research.Arteriosclerosis, thrombosis, and vascular biology · 2016
    Review
  15. Article
  16. Article
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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

3 authors at 2 institutions in 1 country.

F TavnerDepartment of Virology, Faculty of Medicine, Imperial College London, London, UK.
J Frampton
R J Watson
Imperial College London · GBUniversity of Birmingham · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Previous studies have shown that the cell cycle-regulated B-myb promoter contains a conserved E2F binding site that is critical for repressing transcription in quiescent cells. To investigate its significance for permanent promoter silencing, we have inactivated this binding site in the mouse genome. Mice homozygous for the mutant B-mybmE2F allele were fully viable, however, B-myb transcription was derepressed during quiescence in mouse embryo fibroblasts (MEFs) derived from mutant animals. Moreover, it was found that mutation of the E2F site resulted in abnormal maintenance of B-myb expression in senescent MEFs and in differentiated brain tissue. These findings therefore reveal a direct and primary role for repressive E2F complexes in silencing gene expression in post-mitotic cells. Analysis of histone modifications at the promoter showed that histone H3 lysine 9 was constitutively acetylated throughout the cell cycle in homozygous mutant MEFs. This mouse system is the first description of an E2F site mutation in situ and will facilitate the study of E2F function in vivo.

Indexed as

Gene Expression RegulationGene SilencingMitosisAnimalsBinding SitesBlotting, WesternCell CycleCell Cycle ProteinsCells, CulturedChromatin ImmunoprecipitationDNA-Binding ProteinsDNA FootprintingE2F Transcription FactorsEmbryo, MammalianFibroblastsFlow CytometryCell Cycle ProteinsDNA-Binding ProteinsE2F Transcription FactorsMybl2 protein, mouseRNA, MessengerTrans-Activators

Identifiers

PMID17072340
OpenAlexW2012995139

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.