Evidence map›Paper›PMID 24938781›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2014

Loss of Prox1 in striated muscle causes slow to fast skeletal muscle fiber conversion and dilated cardiomyopathy.

Louisa K Petchey, Catherine A Risebro, Joaquim M Vieira, Tom Roberts, John B Bryson, Linda Greensmith, Mark F Lythgoe, Paul R Riley

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

28 citing papers in PubMed, 53 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. PROX1 transcription factor controls rhabdomyosarcoma growth, stemness, myogenic properties and therapeutic targets.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  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

8 authors at 3 institutions in 1 country.

Louisa K PetcheyMolecular Medicine Unit, UCL Institute of Child Health, London WC1N 1EH, United Kingdom;
Catherine A RisebroMolecular Medicine Unit, UCL Institute of Child Health, London WC1N 1EH, United Kingdom;
Joaquim M VieiraMolecular Medicine Unit, UCL Institute of Child Health, London WC1N 1EH, United Kingdom;Department of Physiology, Anatomy and Genetics, University of Oxford, Oxford OX1 3PT, United Kingdom;
Tom RobertsUniversity College London (UCL) Centre for Advanced Biomedical Imaging, London WC1E 6DD, United Kingdom; and.
John B BrysonSobell Department of Motor Neuroscience and Movement Disorders, UCL Institute of Neurology, London WC1N 3BG, United Kingdom.
Linda GreensmithSobell Department of Motor Neuroscience and Movement Disorders, UCL Institute of Neurology, London WC1N 3BG, United Kingdom.
Mark F LythgoeUniversity College London (UCL) Centre for Advanced Biomedical Imaging, London WC1E 6DD, United Kingdom; and.
Paul R RileyMolecular Medicine Unit, UCL Institute of Child Health, London WC1N 1EH, United Kingdom;Department of Physiology, Anatomy and Genetics, University of Oxford, Oxford OX1 3PT, United Kingdom; paul.riley@dpag.ox.ac.uk.
University College London · GBSobell House · GBUniversity of Oxford · GB

Funding

British Heart Foundation PG/09/043/27565Medical Research Council MR/K000608/1
6 · The paper itself

Abstract

Correct regulation of troponin and myosin contractile protein gene isoforms is a critical determinant of cardiac and skeletal striated muscle development and function, with misexpression frequently associated with impaired contractility or disease. Here we reveal a novel requirement for Prospero-related homeobox factor 1 (Prox1) during mouse heart development in the direct transcriptional repression of the fast-twitch skeletal muscle genes troponin T3, troponin I2, and myosin light chain 1. A proportion of cardiac-specific Prox1 knockout mice survive beyond birth with hearts characterized by marked overexpression of fast-twitch genes and postnatal development of a fatal dilated cardiomyopathy. Through conditional knockout of Prox1 from skeletal muscle, we demonstrate a conserved requirement for Prox1 in the repression of troponin T3, troponin I2, and myosin light chain 1 between cardiac and slow-twitch skeletal muscle and establish Prox1 ablation as sufficient to cause a switch from a slow- to fast-twitch muscle phenotype. Our study identifies conserved roles for Prox1 between cardiac and skeletal muscle, specifically implicated in slow-twitch fiber-type specification, function, and cardiomyopathic disease.

Indexed as

AnimalsCardiomyopathy, DilatedCell DifferentiationChromatin ImmunoprecipitationDNA PrimersFluorescent Antibody TechniqueGene Expression Regulation, DevelopmentalHomeodomain ProteinsMiceMice, KnockoutMicroarray AnalysisMuscle, StriatedMyocardiumMyosin Light ChainsProspero-Related Homeobox 1 ProteinReal-Time Polymerase Chain ReactionDNA PrimersHomeodomain ProteinsMLC1A protein, mouseMyosin Light ChainsProspero-Related Homeobox 1 ProteinTroponinTroponin Itroponin T3, skeletal, fast, mouseTumor Suppressor Proteins

Identifiers

PMID24938781
PMCPMC4084422
OpenAlexW2116144300

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.