Evidence map›Paper›PMID 27644006›Full record

ReviewBioEssays : news and reviews in molecular, cellular and developmental biology2016

p53 in the game of transposons.

Annika Wylie, Amanda E Jones, John M Abrams

Open access · greenAbstract readReview
In one paragraph

Review in BioEssays : news and reviews in molecular, cellular and developmental biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
4.8field-weighted citation impact, top 5% 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

17 citing papers in PubMed, 27 citations in OpenAlex.

  1. Review
  2. Review
  3. p53motifDB: integration of genomic information and tumour suppressor p53 binding motifs.Database : the journal of biological databases and curation · 2025
    Article
  4. Review
  5. Affinity-Based Interactome Analysis of Endogenous LINE-1 Macromolecules.Methods in molecular biology (Clifton, N.J.) · 2023
    Article
  6. Virus-Induced Membrane Fusion in Neurodegenerative Disorders.Frontiers in cellular and infection microbiology · 2022
    Review
  7. Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. P53 and Apoptosis in the Drosophila Model.Advances in experimental medicine and biology · 2019
    Review
  13. Transposons, p53 and Genome Security.Trends in genetics : TIG · 2018
    Review
  14. Article
  15. Article
  16. Article
  17. Review
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 1 institution in 1 country.

Annika WylieDepartment of Cell Biology, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Amanda E JonesDepartment of Cell Biology, University of Texas Southwestern Medical Center, Dallas, TX, USA.
John M AbramsDepartment of Cell Biology, University of Texas Southwestern Medical Center, Dallas, TX, USA. john.abrams@utsouthwestern.edu.
The University of Texas Southwestern Medical Center · US

Funding

Molecular and Genetic Control of Programmed Cell DeathR01GM072124 · NIGMS · UT SOUTHWESTERN MEDICAL CENTER · PI ABRAMS, JOHN M · 2004 to 2016
$4.4M
Suppression of mobile elements by p53 genesR01GM115682 · NIGMS · UT SOUTHWESTERN MEDICAL CENTER · PI ABRAMS, JOHN M · 2015 to 2024
$2.7M
A model for deconstructing p53 function in stem cellsF31CA189691 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI WYLIE, ANNIKA DAWN · 2014 to 2015
$50k
NCI NIH HHS F31 CA189691NIGMS NIH HHS R01 GM072124NIGMS NIH HHS R01 GM115682
6 · The paper itself

Abstract

Throughout the animal kingdom, p53 genes function to restrain mobile elements and recent observations indicate that transposons become derepressed in human cancers. Together, these emerging lines of evidence suggest that cancers driven by p53 mutations could represent "transpospoathies," i.e. disease states linked to eruptions of mobile elements. The transposopathy hypothesis predicts that p53 acts through conserved mechanisms to contain transposon movement, and in this way, prevents tumor formation. How transposon eruptions provoke neoplasias is not well understood but, from a broader perspective, this hypothesis also provides an attractive framework to explore unrestrained mobile elements as inciters of late-onset idiopathic disease. Also see the video abstract here.

Indexed as

DNA Transposable ElementsAnimalsHumansMutationNeoplasmsTumor Suppressor Protein p53DNA Transposable ElementsTumor Suppressor Protein p53Drosophilahuman cancersmobile elementsmouse cancer modelsp53piRNAsretrotransposonszebrafish

Identifiers

PMID27644006
PMCPMC5142446
OpenAlexW2521339607

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.