Evidence map›Paper›PMID 11459935›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2001

Regulation of myostatin activity and muscle growth.

S J Lee, A C McPherron

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 661 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
661citing papers in PubMed, 3 pooled it
14.5field-weighted citation impact, top 1% 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

661 citing papers in PubMed, 3 syntheses or guidelines pooled it, 1,583 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Trial
  5. Trial
  6. PasteurizedNutrients · 2024
    Trial
  7. Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Age-Dependent Effect of Myostatin Blockade in theMuscles (Basel, Switzerland) · 2026
    Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article

601 more citing papers are in PubMed but not listed here.

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 2 institutions in 1 country.

S J LeeDepartment of Molecular Biology and Genetics, Johns Hopkins University School of Medicine, 725 North Wolfe Street, Baltimore, MD 21205, USA. sjlee@jhmi.edu
A C McPherron
Johns Hopkins Medicine · USJohns Hopkins University · US

Funding

GDF-8 (MYOSTATIN) AND GDF-11R01HD035887 · NICHD · JOHNS HOPKINS UNIVERSITY · PI LEE, SE-JIN · 1998 to 2007
$2.8M
ROLE OF MYOSTATIN IN CACHEXIAR01CA088866 · NCI · JOHNS HOPKINS UNIVERSITY · PI LEE, SE-JIN · 2001 to 2005
$1.6M
NCI NIH HHS R01 CA088866NCI NIH HHS R01CA88866NICHD NIH HHS R01 HD035887NICHD NIH HHS R01HD35887
6 · The paper itself

Abstract

Myostatin is a transforming growth factor-beta family member that acts as a negative regulator of skeletal muscle mass. To identify possible myostatin inhibitors that may have applications for promoting muscle growth, we investigated the regulation of myostatin signaling. Myostatin protein purified from mammalian cells consisted of a noncovalently held complex of the N-terminal propeptide and a disulfide-linked dimer of C-terminal fragments. The purified C-terminal myostatin dimer was capable of binding the activin type II receptors, Act RIIB and, to a lesser extent, Act RIIA. Binding of myostatin to Act RIIB could be inhibited by the activin-binding protein follistatin and, at higher concentrations, by the myostatin propeptide. To determine the functional significance of these interactions in vivo, we generated transgenic mice expressing high levels of the propeptide, follistatin, or a dominant-negative form of Act RIIB by using a skeletal muscle-specific promoter. Independent transgenic mouse lines for each construct exhibited dramatic increases in muscle mass comparable to those seen in myostatin knockout mice. Our findings suggest that the propeptide, follistatin, or other molecules that block signaling through this pathway may be useful agents for enhancing muscle growth for both human therapeutic and agricultural applications.

Indexed as

Muscle DevelopmentActivin Receptors, Type IIAnimalsCHO CellsCOS CellsCricetinaeFemaleMaleMiceMice, TransgenicMuscle, SkeletalMyostatinProtein BindingReceptors, Growth FactorTransforming Growth Factor betaActivin Receptors, Type IIMSTN protein, humanMstn protein, mouseMyostatinReceptors, Growth FactorTransforming Growth Factor beta

Identifiers

PMID11459935
PMCPMC55416
OpenAlexW2149993139

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.