Evidence map›Paper›PMID 22937058›Full record

ArticlePloS one2012

Proteomic analysis reveals new cardiac-specific dystrophin-associated proteins.

Eric K Johnson, Liwen Zhang, Marvin E Adams, Alistair Phillips, Michael A Freitas, Stanley C Froehner, Kari B Green-Church, Federica Montanaro

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

53 citing papers in PubMed, 83 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Mechanisms of reduced myocardial energetics of the dystrophic heart.American journal of physiology. Heart and circulatory physiology · 2024
    Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Bioinformatic Analysis of the Subproteomic Profile of Cardiomyopathic Tissue.Methods in molecular biology (Clifton, N.J.) · 2023
    Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Duchenne muscular dystrophy.Nature reviews. Disease primers · 2021
    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

8 authors at 3 institutions in 1 country.

Eric K JohnsonCenter for Gene Therapy, The Research Institute at Nationwide Children's Hospital, and the Ohio State University Biochemistry Program, Columbus, Ohio, United States of America.
Liwen Zhang
Marvin E Adams
Alistair Phillips
Michael A Freitas
Stanley C Froehner
Kari B Green-Church
Federica Montanaro
The Ohio State University · USUniversity of Washington · USCincinnati Children's Hospital Medical Center · US

Funding

Signalling via Dystrobrevin in Muscular DystrophyP01NS046788 · NINDS · UNIVERSITY OF WASHINGTON · PI FROEHNER, STANLEY C · 2004 to 2013
$12.8M
Regulation of Syntrophin FunctionR01NS033145 · NINDS · UNIVERSITY OF WASHINGTON · PI FROEHNER, STANLEY C · 1995 to 2013
$5.2M
Acquisition of a high-throughput high mass accuracy MS for chromatin researchS10RR023647 · NCRR · OHIO STATE UNIVERSITY · PI FREITAS, MICHAEL A · 2007 to 2007
$500k
NCRR NIH HHS S10 RR023647NINDS NIH HHS P01 NS046788NINDS NIH HHS R01 NS033145NINDS NIH HHS R01 NS33145
6 · The paper itself

Abstract

Mutations affecting the expression of dystrophin result in progressive loss of skeletal muscle function and cardiomyopathy leading to early mortality. Interestingly, clinical studies revealed no correlation in disease severity or age of onset between cardiac and skeletal muscles, suggesting that dystrophin may play overlapping yet different roles in these two striated muscles. Since dystrophin serves as a structural and signaling scaffold, functional differences likely arise from tissue-specific protein interactions. To test this, we optimized a proteomics-based approach to purify, identify and compare the interactome of dystrophin between cardiac and skeletal muscles from as little as 50 mg of starting material. We found selective tissue-specific differences in the protein associations of cardiac and skeletal muscle full length dystrophin to syntrophins and dystrobrevins that couple dystrophin to signaling pathways. Importantly, we identified novel cardiac-specific interactions of dystrophin with proteins known to regulate cardiac contraction and to be involved in cardiac disease. Our approach overcomes a major challenge in the muscular dystrophy field of rapidly and consistently identifying bona fide dystrophin-interacting proteins in tissues. In addition, our findings support the existence of cardiac-specific functions of dystrophin and may guide studies into early triggers of cardiac disease in Duchenne and Becker muscular dystrophies.

Indexed as

DystrophinDystrophin-Associated ProteinsHumansImmunoprecipitationMass SpectrometryMuscle, SkeletalMyocardiumProtein BindingProteomicsSignal TransductionTandem Mass SpectrometryDystrophinDystrophin-Associated Proteins

Identifiers

PMID22937058
PMCPMC3427372
OpenAlexW2044462734

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.