Evidence map›Paper›PMID 24019467›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2013

Regulation of GDF-11 and myostatin activity by GASP-1 and GASP-2.

Yun-Sil Lee, Se-Jin Lee

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

59 citing papers in PubMed, 95 citations in OpenAlex.

  1. Article
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  8. Article
  9. Myostatin: A Skeletal Muscle Chalone.Annual review of physiology · 2023
    Review
  10. Association of a variant upstream ofTranslational animal science · 2023
    Article
  11. Skeletal Muscle Regeneration in Cardiotoxin-Induced Muscle Injury Models.International journal of molecular sciences · 2022
    Review
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
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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.

Yun-Sil LeeDepartment of Molecular Biology and Genetics, Johns Hopkins University School of Medicine, Baltimore, MD 21205.
Se-Jin Lee
Johns Hopkins Medicine · US

Funding

Regulation of TGF - (beta) pathways in muscular dystrophy fibrosisP01NS072027 · NINDS · UNIVERSITY OF CHICAGO · PI HEYDEMANN, AHLKE · 2011 to 2015
$6.2M
Characterization of Myostatin and GDF-11R01AR060636 · NIAMS · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI LEE, SE-JIN · 2010 to 2020
$3.7M
Mechanisms Underlying Myostatin Regulation and ActivityR01AR059685 · NIAMS · JOHNS HOPKINS UNIVERSITY · PI LEE, SE-JIN · 2010 to 2014
$1.7M
NIAMS NIH HHS R01 AR059685NIAMS NIH HHS R01AR059685NIAMS NIH HHS R01 AR060636NIAMS NIH HHS R01AR060636NINDS NIH HHS P01NS0720027NINDS NIH HHS P01 NS072027
6 · The paper itself

Abstract

Myostatin (MSTN) and growth and differentiation factor-11 (GDF-11) are highly related TGF-β family members that have distinct biological functions. MSTN is expressed primarily in skeletal muscle and acts to limit muscle growth. GDF-11 is expressed more widely and plays multiple roles, including regulating axial skeletal patterning during development. Several MSTN and GDF-11 binding proteins have been identified, including GDF-associated serum protein-1 (GASP-1) and GASP-2, which are capable of inhibiting the activities of these ligands. Here, we show that GASP-1 and GASP-2 act by blocking the initial signaling event (namely, the binding of the ligand to the type II receptor). Moreover, we show that mice lacking Gasp1 and Gasp2 have phenotypes consistent with overactivity of MSTN and GDF-11. Specifically, we show that Gasp2(-/-) mice have posteriorly directed transformations of the axial skeleton, which contrast with the anteriorly directed transformations seen in Gdf11(-/-) mice. We also show that both Gasp1(-/-) and Gasp2(-/-) mice have reductions in muscle weights, a shift in fiber type from fast glycolytic type IIb fibers to fast oxidative type IIa fibers, and impaired muscle regeneration ability, which are the reverse of what are seen in Mstn(-/-) mice. All of these findings suggest that both GASP-1 and GASP-2 are important modulators of GDF-11 and MSTN activity in vivo.

Indexed as

AnimalsBody PatterningBone and BonesBone Morphogenetic ProteinsCardiotoxinsCarrier ProteinsFollistatinGene Expression ProfilingGene Expression RegulationGrowth Differentiation FactorsIntracellular Signaling Peptides and ProteinsMiceMice, Inbred C57BLMice, Mutant StrainsMuscle Fibers, SkeletalMutationBone Morphogenetic ProteinsCardiotoxinsCarrier ProteinsFollistatinGdf11 protein, mouseGprasp1 protein, mouseGprasp2 protein, mouseGrowth Differentiation FactorsIntracellular Signaling Peptides and ProteinsMyostatinProtein Serine-Threonine KinasesReceptors, G-Protein-CoupledReceptors, Transforming Growth Factor betaReceptor, Transforming Growth Factor-beta Type II

Identifiers

PMID24019467
PMCPMC3785741
OpenAlexW2052145926

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.