ArticleThe Journal of clinical investigation1997
Integrins (alpha7beta1) in muscle function and survival. Disrupted expression in merosin-deficient congenital muscular dystrophy.
Article in The Journal of clinical investigation, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.
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Who cites it
57 citing papers in PubMed, 1 synthesis or guideline pooled it, 184 citations in OpenAlex.
- Genetic and Clinical Advances of Congenital Muscular Dystrophy.Chinese medical journal · 2017Pooled it
- Spatial proteomics reveals recombinant human laminin-111 restores adhesion signaling to laminin-α2-deficient muscle.JCI insight · 2025Article
- Aptamer-conjugated gold nanoparticles enable oligonucleotide delivery into muscle stem cells to promote regeneration of dystrophic muscles.Nature communications · 2025Article
- Culture substrate stiffness impacts human myoblast contractility-dependent proliferation and nuclear envelope wrinkling.Journal of cell science · 2024Article
- Limb girdle muscular dystrophy 23 caused by compound heterozygous mutations ofFrontiers in pediatrics · 2023Article
- Integrin α7 Mutations Are Associated With Adult-Onset Cardiac Dysfunction in Humans and Mice.Journal of the American Heart Association · 2022Article
- Novel γ-sarcoglycan interactors in murine muscle membranes.Skeletal muscle · 2022Article
- Costameric integrin and sarcoglycan protein levels are altered in aMolecular biology of the cell · 2021Article
- A Family of Laminin α2 Chain-Deficient Mouse Mutants: Advancing the Research on LAMA2-CMD.Frontiers in molecular neuroscience · 2020Review
- Laminin and Integrin in LAMA2-Related Congenital Muscular Dystrophy: From Disease to Therapeutics.Frontiers in molecular neuroscience · 2020Article
- Current understanding and treatment of cardiac and skeletal muscle pathology in laminin-α2 chain-deficient congenital muscular dystrophy.The application of clinical genetics · 2019Article
- Impaired fetal muscle development and JAK-STAT activation mark disease onset and progression in a mouse model for merosin-deficient congenital muscular dystrophy.Human molecular genetics · 2017Article
- Integrin α7: a major driver and therapeutic target for glioblastoma malignancy.Stem cell investigation · 2017Article
- Deletion of integrin α7 subunit does not aggravate the phenotype of laminin α2 chain-deficient mice.Scientific reports · 2015Article
- Hanging on for the ride: adhesion to the extracellular matrix mediates cellular responses in skeletal muscle morphogenesis and disease.Developmental biology · 2015Review
- Immobilization of Dystrophin and Laminin α2-Chain Deficient Zebrafish Larvae In Vivo Prevents the Development of Muscular Dystrophy.PloS one · 2015Article
- Quantitative proteomic analysis reveals metabolic alterations, calcium dysregulation, and increased expression of extracellular matrix proteins in laminin α2 chain-deficient muscle.Molecular & cellular proteomics : MCP · 2014Article
- Laminin-111 improves muscle repair in a mouse model of merosin-deficient congenital muscular dystrophy.Human molecular genetics · 2014Article
- Suppression of anoikis in human intestinal epithelial cells: differentiation state-selective roles of α2β1, α3β1, α5β1, and α6β4 integrins.BMC cell biology · 2013Article
- Integrins protect cardiomyocytes from ischemia/reperfusion injury.The Journal of clinical investigation · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 4 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations in genes coding for dystrophin, for alpha, beta, gamma, and delta-sarcoglycans, or for the alpha2 chain of the basement membrane component merosin (laminin-2/4) cause various forms of muscular dystrophy. Analyses of integrins showed an abnormal expression and localization of alpha7beta1 isoforms in myofibers of merosin-deficient human patients and mice, but not in dystrophin-deficient or sarcoglycan-deficient humans and animals. It was shown previously that skeletal muscle fibers require merosin for survival and function (Vachon, P.H., F. Loechel, H. Xu, U.M. Wewer, and E. Engvall. 1996. J. Cell Biol. 134:1483-1497). Correction of merosin deficiency in vitro through cell transfection with the merosin alpha2 chain restored the normal localization of alpha7beta1D integrins as well as myotube survival. Overexpression of the apoptosis-suppressing molecule Bcl-2 also promoted the survival of merosin-deficient myotubes, but did not restore a normal expression of alpha7beta1D integrins. Blocking of beta1 integrins in normal myotubes induced apoptosis and severely reduced their survival. These findings (a) identify alpha7beta1D integrins as the de facto receptors for merosin in skeletal muscle; (b) indicate a merosin dependence for the accurate expression and membrane localization of alpha7beta1D integrins in myofibers; (c) provide a molecular basis for the critical role of merosin in myofiber survival; and (d) add new insights to the pathogenesis of neuromuscular disorders.
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