Evidence map›Paper›PMID 21858002›Full record

ArticlePloS one2011

Increased muscle stress-sensitivity induced by selenoprotein N inactivation in mouse: a mammalian model for SEPN1-related myopathy.

Mathieu Rederstorff, Perrine Castets, Sandrine Arbogast, Jeanne Lainé, Stéphane Vassilopoulos, Maud Beuvin, Odile Dubourg, Alban Vignaud, Arnaud Ferry, Alain Krol and 4 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

36 citing papers in PubMed, 75 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. "Alphabet" Selenoproteins: Their Characteristics and Physiological Roles.International journal of molecular sciences · 2023
    Review
  8. Article
  9. Review
  10. Review
  11. Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. 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

14 authors at 7 institutions in 1 country.

Mathieu RederstorffArchitecture et Réactivité de l'ARN, Université de Strasbourg, CNRS, IBMC, Strasbourg, France.
Perrine Castets
Sandrine Arbogast
Jeanne Lainé
Stéphane Vassilopoulos
Maud Beuvin
Odile Dubourg
Alban Vignaud
Arnaud Ferry
Alain Krol
Valérie Allamand
Pascale Guicheney
Ana Ferreiro
Alain Lescure
Inserm · FRInstitut de Myologie · FRUniversité de Strasbourg · FRArchitecture et Réactivité de l'arN · FRCentre National de la Recherche Scientifique · FRSorbonne Université · FRUniversité Paris Cité · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Selenium is an essential trace element and selenoprotein N (SelN) was the first selenium-containing protein shown to be directly involved in human inherited diseases. Mutations in the SEPN1 gene, encoding SelN, cause a group of muscular disorders characterized by predominant affection of axial muscles. SelN has been shown to participate in calcium and redox homeostasis, but its pathophysiological role in skeletal muscle remains largely unknown. To address SelN function in vivo, we generated a Sepn1-null mouse model by gene targeting. The Sepn1(-/-) mice had normal growth and lifespan, and were macroscopically indistinguishable from wild-type littermates. Only minor defects were observed in muscle morphology and contractile properties in SelN-deficient mice in basal conditions. However, when subjected to challenging physical exercise and stress conditions (forced swimming test), Sepn1(-/-) mice developed an obvious phenotype, characterized by limited motility and body rigidity during the swimming session, as well as a progressive curvature of the spine and predominant alteration of paravertebral muscles. This induced phenotype recapitulates the distribution of muscle involvement in patients with SEPN1-Related Myopathy, hence positioning this new animal model as a valuable tool to dissect the role of SelN in muscle function and to characterize the pathophysiological process.

Indexed as

AnimalsDisease Models, AnimalEmbryo, MammalianFemaleGene Expression Regulation, DevelopmentalImmunoblottingMaleMiceMice, 129 StrainMice, Inbred C57BLMice, KnockoutMice, TransgenicMotor ActivityMuscle ContractionMuscle ProteinsMuscle, SkeletalMuscle ProteinsSelenoproteinsSEPN1 protein, mouse

Identifiers

PMID21858002
PMCPMC3152547
OpenAlexW2087944893

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.