Evidence map›Paper›PMID 26634192›Full record

ArticleJournal of neuromuscular diseases

Mammalian Mss51 is a skeletal muscle-specific gene modulating cellular metabolism.

Adam L Moyer, Kathryn R Wagner

Open access · bronzeAbstract read
In one paragraph

Article in Journal of neuromuscular diseases. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

20 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. Review
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  9. Article
  10. Current and Future Therapeutic Strategies for Limb Girdle Muscular Dystrophy Type R1: Clinical and Experimental Approaches.Pathophysiology : the official journal of the International Society for Pathophysiology · 2021
    Review
  11. Article
  12. Article
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  14. Article
  15. Article
  16. Article
  17. Article
  18. AEMBO reports · 2017
    Article
  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

2 authors at 1 institution in 1 country.

Adam L MoyerThe Hugo W. Moser Research Institute, Kennedy Krieger Institute, Baltimore, MD 21205 ; Graduate Program in Cellular and Molecular Medicine, Johns Hopkins School of Medicine, Baltimore, MD 21287.
Kathryn R WagnerThe Hugo W. Moser Research Institute, Kennedy Krieger Institute, Baltimore, MD 21205 ; Graduate Program in Cellular and Molecular Medicine, Johns Hopkins School of Medicine, Baltimore, MD 21287 ; Departments of Neurology and Neuroscience, Johns Hopkins School of Medicine, Baltimore, MD 21287.
Kennedy Krieger Institute · US

Funding

ZINC AND CA EDTA THERAPY OF PLUMBISMM01RR000052 · NCRR · JOHNS HOPKINS UNIVERSITY · PI BELCHER, HAROLYN MILLICENT EDITH · 1985 to 2007
$37.3M
Training and education CoreU54AR052646 · NIAMS · UNIVERSITY OF PENNSYLVANIA · PI MCNALLY, ELIZABETH M, SWEENEY, H LEE · 2005 to 2020
$24.1M
Myogenesis Studies for FSHD BiomarkersU54HD060848 · NICHD · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI EMERSON, CHARLES P. · 2008 to 2017
$16.1M
Partnering to treat an Orphan Disease Duchenne Muscular DystrophyUH2TR000966 · NCATS · HUGO W. MOSER RES INST KENNEDY KRIEGER · PI FROEHNER, STANLEY C, WAGNER, KATHRYN R. · 2013 to 2013
$2.9M
Myostatin in Muscle Growth and RegenerationK08NS002212 · NINDS · JOHNS HOPKINS UNIVERSITY · PI WAGNER, KATHRYN R · 2001 to 2005
$657k
A Novel Xenograft Mouse Model of Facioscapulohumeral Muscular DystrophyR21NS079529 · NINDS · HUGO W. MOSER RES INST KENNEDY KRIEGER · PI WAGNER, KATHRYN R. · 2012 to 2013
$440k
NCATS NIH HHS UH2 TR000966NCRR NIH HHS M01 RR000052NIAMS NIH HHS U54 AR052646NICHD NIH HHS U54 HD060848NINDS NIH HHS K08 NS002212NINDS NIH HHS R21 NS079529
6 · The paper itself

Abstract

backgroundThe transforming growth factor β (TGF-β) signaling pathways modulate skeletal muscle growth, regeneration, and cellular metabolism. Several recent gene expression studies have shown that inhibition of myostatin and TGF-β1 signaling consistently leads to a significant reduction in expression of Mss51, also named Zmynd17. The function of mammalian Mss51 is unknown although a putative homolog in yeast is a mitochondrial translational activator.

objectiveThe objective of this work was to characterize mammalian Mss51.

methodsQuantitative RT-PCR and immunoblot of subcellular fractionation were used to determine expression patterns and localization of Mss51. The CRISPR/Cas9 system was used to reduce expression of Mss51 in C2C12 myoblasts and the function of Mss51 was evaluated in assays of proliferation, differentiation and cellular metabolism.

resultsMss51 was predominantly expressed in skeletal muscle and in those muscles dominated by fast-twitch fibers.

conclusions

Indexed as

metabolismmitochondriaMss51myostatinmyotubeskeletal muscleTGF-β

Identifiers

PMID26634192
PMCPMC4664537
OpenAlexW1853391860

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.