ArticleThe Journal of cell biology2012
Sarcospan-dependent Akt activation is required for utrophin expression and muscle regeneration.
Article in The Journal of cell biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 60 citations in OpenAlex.
- Mitochondrial alterations and oxidative stress in an acute transient mouse model of muscle degeneration: implications for muscular dystrophy and related muscle pathologies.The Journal of biological chemistry · 2014Trial
- Article
- The Development of Robust Antibodies to Sarcospan, a Dystrophin- and Integrin-Associated Protein, for Basic and Translational Research.International journal of molecular sciences · 2024Article
- Myoscaffolds reveal laminin scarring is detrimental for stem cell function while sarcospan induces compensatory fibrosis.NPJ Regenerative medicine · 2023Article
- Multi-omics analysis of sarcospan overexpression in mdx skeletal muscle reveals compensatory remodeling of cytoskeleton-matrix interactions that promote mechanotransduction pathways.Skeletal muscle · 2023Article
- High-Throughput Screening to Identify Modulators of Sarcospan.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Skeletal Muscle Regeneration in Cardiotoxin-Induced Muscle Injury Models.International journal of molecular sciences · 2022Review
- Sarcospan increases laminin-binding capacity of α-dystroglycan to ameliorate DMD independent of Galgt2.Human molecular genetics · 2022Article
- Cellular pathology of the human heart in Duchenne muscular dystrophy (DMD): lessons learned from in vitro modeling.Pflugers Archiv : European journal of physiology · 2021Review
- Loss of sarcospan exacerbates pathology in mdx mice, but does not affect utrophin amelioration of disease.Human molecular genetics · 2021Article
- PDE10A Inhibition Reduces the Manifestation of Pathology in DMD Zebrafish and Represses the Genetic Modifier PITPNA.Molecular therapy : the journal of the American Society of Gene Therapy · 2021Article
- High-throughput screening identifies modulators of sarcospan that stabilize muscle cells and exhibit activity in the mouse model of Duchenne muscular dystrophy.Skeletal muscle · 2020Article
- Sestrins are evolutionarily conserved mediators of exercise benefits.Nature communications · 2020Article
- Development of a high-throughput screen to identify small molecule enhancers of sarcospan for the treatment of Duchenne muscular dystrophy.Skeletal muscle · 2019Article
- Stabilization of the cardiac sarcolemma by sarcospan rescues DMD-associated cardiomyopathy.JCI insight · 2019Article
- Protein disulfide isomerase as a prosurvival factor in cell therapy for muscular and vascular diseases.Stem cell research & therapy · 2018Article
- PPARβ/δ: Linking Metabolism to Regeneration.International journal of molecular sciences · 2018Review
- Efficacy of Prednisolone in Generated Myotubes Derived From Fibroblasts of Duchenne Muscular Dystrophy Patients.Frontiers in pharmacology · 2018Article
- Genetic modifiers of Duchenne and facioscapulohumeral muscular dystrophies.Muscle & nerve · 2018Review
- Lectin-binding characterizes the healthy human skeletal muscle glycophenotype and identifies disease-specific changes in dystrophic muscle.Glycobiology · 2017Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
Utrophin is normally confined to the neuromuscular junction (NMJ) in adult muscle and partially compensates for the loss of dystrophin in mdx mice. We show that Akt signaling and utrophin levels were diminished in sarcospan (SSPN)-deficient muscle. By creating several transgenic and knockout mice, we demonstrate that SSPN regulates Akt signaling to control utrophin expression. SSPN determined α-dystroglycan (α-DG) glycosylation by affecting levels of the NMJ-specific glycosyltransferase Galgt2. After cardiotoxin (CTX) injury, regenerating myofibers express utrophin and Galgt2-modified α-DG around the sarcolemma. SSPN-null mice displayed delayed differentiation after CTX injury caused by loss of utrophin and Akt signaling. Treatment of SSPN-null mice with viral Akt increased utrophin and restored muscle repair after injury, revealing an important role for the SSPN-Akt-utrophin signaling axis in regeneration. SSPN improved cell surface expression of utrophin by increasing transportation of utrophin and DG from endoplasmic reticulum/Golgi membranes. Our experiments reveal functions of utrophin in regeneration and new pathways that regulate utrophin expression at the cell surface.
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Registered trials
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.