Evidence map›Paper›PMID 23407451›Full record

ArticleEndocrinology2013

The pro-forms of insulin-like growth factor I (IGF-I) are predominant in skeletal muscle and alter IGF-I receptor activation.

Julia Durzyńska, Anastassios Philippou, Becky K Brisson, Michelle Nguyen-McCarty, Elisabeth R Barton

Open access · bronzeAbstract read
In one paragraph

Article in Endocrinology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.7field-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

35 citing papers in PubMed, 58 citations in OpenAlex.

  1. Review
  2. Impaired myoblast differentiation and muscle IGF-1 receptor signaling pathway activation after N-glycosylation inhibition.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
    Article
  3. Ablation of specific insulin-like growth factor I forms reveals the importance of cleavage for regenerative capacity and glycosylation for skeletal muscle storage.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
    Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Actions and interactions of IGF-I and MMPs during muscle regeneration.Seminars in cell & developmental biology · 2021
    Review
  10. Article
  11. Article
  12. The Effects of Muscle Cell Aging on Myogenesis.International journal of molecular sciences · 2021
    Article
  13. Review
  14. Review
  15. Matrix Metalloproteinase 13 from Satellite Cells is Required for Efficient Muscle Growth and Regeneration.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2020
    Article
  16. Article
  17. Article
  18. Article
  19. Deletion of muscle IGF-I transiently impairs growth and progressively disrupts glucose homeostasis in male mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article
  20. Article
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

5 authors at 1 institution in 1 country.

Julia DurzyńskaDepartment of Anatomy and Cell Biology, School of Dental Medicine, and Pennsylvania Muscle Institute, University of Pennsylvania, Philadelphia, PA 19104, USA.
Anastassios Philippou
Becky K Brisson
Michelle Nguyen-McCarty
Elisabeth R Barton
University of Pennsylvania · US

Funding

Training in Muscle Biology and Muscle DiseaseT32AR053461 · NIAMS · UNIVERSITY OF PENNSYLVANIA · PI OSTAP, E. MICHAEL · 2006 to 2025
$4.9M
Modulation of Muscle Regenerationby Growth FactorsR01AR057363 · NIAMS · UNIVERSITY OF PENNSYLVANIA · PI BARTON, ELISABETH R · 2010 to 2014
$1.4M
NIAMS NIH HHS AR053461NIAMS NIH HHS AR057363NIAMS NIH HHS R01 AR057363NIAMS NIH HHS T32 AR053461
6 · The paper itself

Abstract

IGF-I is a key regulator of muscle development and growth. The pre-pro-peptide produced by the Igf1gene undergoes several posttranslational processing steps to result in a secreted mature protein, which is thought to be the obligate ligand for the IGF-I receptor (IGF-IR). The goals of this study were to determine what forms of IGF-I exist in skeletal muscle, and whether the mature IGF-I protein was the only form able to activate the IGF-IR. We measured the proportion of IGF-I species in murine skeletal muscle and found that the predominant forms were nonglycosylated pro-IGF-I and glycosylated pro-IGF-I, which retained the C-terminal E peptide extension, instead of mature IGF-I. These forms were validated using samples subjected to viral expression of IGF-I combined with furin and glycosidase digestion. To determine whether the larger molecular weight IGF-I forms were also ligands for the IGF-IR, we generated each specific form through transient transfection of 3T3 cells and used the enriched media to perform kinase receptor activation assays. Compared with mature IGF-I, nonglycosylated pro-IGF-I had similar ability to activate the IGF-IR, whereas glycosylation of pro-IGF-I significantly reduced receptor activation. Thus, it is important to understand not only the quantity, but also the proportion of IGF-I forms produced, to evaluate the true biological activity of this growth factor.

Indexed as

3T3 CellsAnimalsFurinGlycosylationInsulin-Like Growth Factor IMiceMice, Inbred C57BLMolecular WeightMuscle, SkeletalProtein PrecursorsProtein Processing, Post-TranslationalReceptor, IGF Type 1Recombinant ProteinsTransfectionFurinInsulin-Like Growth Factor Ipro-insulin-like growth factor IProtein PrecursorsReceptor, IGF Type 1Recombinant Proteins

Identifiers

PMID23407451
PMCPMC3578996
OpenAlexW1992540316

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.