Evidence map›Paper›PMID 21216283›Full record

ArticleBiochimica et biophysica acta2011

Activation of AKT signaling promotes cell growth and survival in α7β1 integrin-mediated alleviation of muscular dystrophy.

Marni D Boppart, Dean J Burkin, Stephen J Kaufman

Open access · greenAbstract read
In one paragraph

Article in Biochimica et biophysica acta, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.5field-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

37 citing papers in PubMed, 60 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Review
  9. The Role of MicroRNA in the Pathogenesis of Duchenne Muscular Dystrophy.International journal of molecular sciences · 2024
    Review
  10. Article
  11. Article
  12. Mechanisms of exercise as a preventative measure to muscle wasting.American journal of physiology. Cell physiology · 2021
    Review
  13. Review
  14. Article
  15. Article
  16. Integrin signaling: linking mechanical stimulation to skeletal muscle hypertrophy.American journal of physiology. Cell physiology · 2019
    Review
  17. Article
  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

3 authors at 1 institution in 1 country.

Marni D BoppartDepartment of Kinesiology and Community Health, University of Illinois, Urbana, IL 61801, USA. mboppart@illinois.edu
Dean J Burkin
Stephen J Kaufman
Illinois Department of Public Health · US

Funding

Role of the Alpha 7 Beta 1 Integrin in Muscle IntegrityR01AG014632 · NIA · UNIVERSITY OF ILLINOIS URBANA-CHAMPAIGN · PI KAUFMAN, STEPHEN · 1997 to 2005
$1.8M
Integrin Alleviation of Muscular DystrophyR01AR053697 · NIAMS · UNIVERSITY OF NEVADA RENO · PI BURKIN, DEAN J. · 2008 to 2012
$1.2M
NIAMS NIH HHS R01 AR053697NIAMS NIH HHS R01AR053697NIA NIH HHS R01 AG014632NIA NIH HHS R01AG014632
6 · The paper itself

Abstract

Transgenic expression of the α7 integrin can ameliorate muscle pathology in a mouse model of Duchenne muscular dystrophy (mdx/utr(-/-)) and thus can compensate for the loss of dystrophin in diseased mice. In spite of the beneficial effects of the α7 integrin in protecting mice from dystrophy, identification of molecular signaling events responsible for these changes remains to be established. The purpose of this study was to determine a role for signaling in the amelioration of muscular dystrophy by α7 integrin. Activation of PI3K, ILK, AKT, mTOR, p70S6K, BAD, ERK, and p38 was measured in the muscle from wild type (WT), mdx/utr(-/-) and α7BX2-mdx/utr(-/-) mice using in vitro activity assays or phosphospecific antibodies and western blotting. Significant increases in PI3K activity (47%), ILK activity (2.0-fold), mTOR (Ser2448) (57%), p70S6K (Thr389) (11.7-fold), and ERK (Thr202/Tyr204) (66%) were demonstrated in dystrophic mdx/utr(-/-) muscle compared to WT. A significant decrease in p38 phosphorylation (2.9-fold) was also observed. Although most of these signaling events were similar in dystrophic mdx/utr(-/-) mice overexpressing the α7 integrin, the AKT (Ser473):AKT ratio (2-fold vs. WT) and p70S6K phosphorylation (18-fold vs. WT) were higher in α7BX2-mdx/utr(-/-) compared to mdx/utr(-/-) mice. In addition, increased phosphorylation of BAD Serine 112 may contribute to the significant reduction in TUNEL(+) cells observed in α7BX2-mdx/utr(-/-) mice. We conclude that the α7β1 integrin confers a protective effect in dystrophic muscle through the activation of the ILK, AKT, p70S6K and BAD signaling to promote muscle cell survival.

Indexed as

AnimalsApoptosisGene Expression RegulationIntegrinsMiceMice, Inbred mdxMice, TransgenicMuscle, SkeletalMuscular Dystrophy, Duchennep38 Mitogen-Activated Protein KinasesPhosphorylationProtein Serine-Threonine KinasesProto-Oncogene Proteins c-aktRibosomal Protein S6 Kinases, 70-kDaScaffold Protein ILKSignal Transductionintegrin alpha7beta1Integrinsp38 Mitogen-Activated Protein KinasesProtein Serine-Threonine KinasesProto-Oncogene Proteins c-aktRibosomal Protein S6 Kinases, 70-kDaScaffold Protein ILK

Identifiers

PMID21216283
PMCPMC3046458
OpenAlexW2137082747

What OpenQuestion holds

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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.