Evidence map›Paper›PMID 18055553›Full record

ArticleThe American journal of pathology2007

Deletion of integrin-linked kinase from skeletal muscles of mice resembles muscular dystrophy due to alpha 7 beta 1-integrin deficiency.

Ania L Gheyara, Ainara Vallejo-Illarramendi, Keling Zang, Lin Mei, Rene St-Arnaud, Shoukat Dedhar, Louis F Reichardt

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.5field-weighted citation impact, top 20% 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

25 citing papers in PubMed, 41 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Integrin signaling: linking mechanical stimulation to skeletal muscle hypertrophy.American journal of physiology. Cell physiology · 2019
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. The extracellular matrix and insulin resistance.Trends in endocrinology and metabolism: TEM · 2015
    Review
  16. Article
  17. Review
  18. Article
  19. 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

7 authors at 4 institutions in 2 countries.

Ania L GheyaraDepartment of Pathology, University of California, San Francisco, San Francisco, California 94143, USA.
Ainara Vallejo-Illarramendi
Keling Zang
Lin Mei
Rene St-Arnaud
Shoukat Dedhar
Louis F Reichardt
University of California, San Francisco · USAugusta University · USMcGill University · CAUniversity of British Columbia · CA

Funding

STUDIES ON A NEURTITE OUTGROWTH FACTORR01NS019090 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI REICHARDT, LOUIS FRENCH · 1985 to 2009
$3.4M
The Role of Integrin Linked Kinase in Skeletal MuscleF32AR051669 · NIAMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI GHEYARA, ANIA LESELA · 2004 to 2006
$165k
NIAMS NIH HHS F32 AR051669NINDS NIH HHS R01 NS019090NINDS NIH HHS R01NS19090
6 · The paper itself

Abstract

Integrin-linked kinase (Ilk) is a serine/threonine kinase and an adaptor protein that links integrins to the actin cytoskeleton and to a number of signaling pathways involved in integrin action. We hypothesized that Ilk may act as an important effector of integrins in skeletal muscle, where these receptors provide a critical link between the sarcolemma and the extracellular matrix. Using the cre/lox system, we deleted Ilk from skeletal muscles of mice. The resulting mutants developed a progressive muscular dystrophy with multiple degenerating and regenerating muscle fibers, increased central nuclei, and endomysial fibrosis. These defects were widespread but were most severe near myofascial junctions where Ilk mutants showed displacement of focal adhesion-related proteins, including vinculin, paxillin, focal adhesion kinase, dystrophin, and the alpha 7 beta 1D-integrin subunits. Distal ends of mutant muscle fibers appeared irregular, and there was restructuring of the actin cytoskeleton. These findings resemble those seen in humans and mice lacking the alpha 7-integrin subunit and suggest that Ilk may act as a cytoplasmic effector of alpha 7 beta1-integrin in the pathogenesis of these deficiencies.

Indexed as

AnimalsFocal AdhesionsIntegrinsMiceMice, KnockoutMuscle, SkeletalMuscular DystrophiesMutationProtein Serine-Threonine KinasesScaffold Protein ILKintegrin alpha7beta1IntegrinsProtein Serine-Threonine KinasesScaffold Protein ILK

Identifiers

PMID18055553
PMCPMC2111119
OpenAlexW2095790139

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.