Evidence map›Paper›PMID 25208565›Full record

ArticleMolecular biology of the cell2014

The RNA-binding protein Staufen1 impairs myogenic differentiation via a c-myc-dependent mechanism.

Aymeric Ravel-Chapuis, Tara E Crawford, Marie-Laure Blais-Crépeau, Guy Bélanger, Chase T Richer, Bernard J Jasmin

Open access · greenAbstract read
In one paragraph

Article in Molecular biology of the cell, 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
1.6field-weighted citation impact, top 17% 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, 33 citations in OpenAlex.

  1. Article
  2. Article
  3. New Horizons in Myotonic Dystrophy Type 1: Cellular Senescence as a Therapeutic Target.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025
    Review
  4. Article
  5. Review
  6. Skeletal Muscle Regeneration in Cardiotoxin-Induced Muscle Injury Models.International journal of molecular sciences · 2022
    Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Frontiers in neurology · 2018
    Review
  17. Staufen1 inhibits MyoD translation to actively maintain muscle stem cell quiescence.Proceedings of the National Academy of Sciences of the United States of America · 2017
    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

6 authors at 1 institution in 1 country.

Aymeric Ravel-ChapuisDepartment of Cellular and Molecular Medicine, Faculty of Medicine, University of Ottawa, Ottawa, ON K1H 8M5, Canada.
Tara E CrawfordDepartment of Cellular and Molecular Medicine, Faculty of Medicine, University of Ottawa, Ottawa, ON K1H 8M5, Canada.
Marie-Laure Blais-CrépeauDepartment of Cellular and Molecular Medicine, Faculty of Medicine, University of Ottawa, Ottawa, ON K1H 8M5, Canada.
Guy BélangerDepartment of Cellular and Molecular Medicine, Faculty of Medicine, University of Ottawa, Ottawa, ON K1H 8M5, Canada.
Chase T RicherDepartment of Cellular and Molecular Medicine, Faculty of Medicine, University of Ottawa, Ottawa, ON K1H 8M5, Canada.
Bernard J JasminDepartment of Cellular and Molecular Medicine, Faculty of Medicine, University of Ottawa, Ottawa, ON K1H 8M5, Canada jasmin@uottawa.ca.
University of Ottawa · CA

Funding

Canadian Institutes of Health Research
6 · The paper itself

Abstract

Recent work has shown that Staufen1 plays key roles in skeletal muscle, yet little is known about its pattern of expression during embryonic and postnatal development. Here we first show that Staufen1 levels are abundant in mouse embryonic muscles and that its expression decreases thereafter, reaching low levels in mature muscles. A similar pattern of expression is seen as cultured myoblasts differentiate into myotubes. Muscle degeneration/regeneration experiments revealed that Staufen1 increases after cardiotoxin injection before returning to the low levels seen in mature muscles. We next prevented the decrease in Staufen1 during differentiation by generating stable C2C12 muscle cell lines overexpressing Staufen1. Cells overexpressing Staufen1 differentiated poorly, as evidenced by reductions in the differentiation and fusion indices and decreases in MyoD, myogenin, MEF2A, and MEF2C, independently of Staufen-mediated mRNA decay. However, levels of c-myc, a factor known to inhibit differentiation, were increased in C2C12 cells overexpressing Staufen1 through enhanced translation. By contrast, the knockdown of Staufen1 decreased c-myc levels in myoblasts. Collectively our results show that Staufen1 is highly expressed during early stages of differentiation/development and that it can impair differentiation by regulating c-myc, thereby highlighting the multifunctional role of Staufen1 in skeletal muscle cells.

Indexed as

Muscle DevelopmentAnimalsCell DifferentiationGene Expression Regulation, DevelopmentalMEF2 Transcription FactorsMiceMusclesMyoD ProteinProto-Oncogene Proteins c-mycRegenerationRNA-Binding ProteinsMef2a protein, mouseMef2c protein, mouseMEF2 Transcription FactorsMyc protein, mouseMyoD1 myogenic differentiation proteinMyoD ProteinProto-Oncogene Proteins c-mycRNA-Binding ProteinsStau1 protein, mouse

Identifiers

PMID25208565
PMCPMC4230783
OpenAlexW2144672824

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.