ArticleHuman molecular genetics2015
Gamma-sarcoglycan is required for the response of archvillin to mechanical stimulation in skeletal muscle.
Article in Human molecular genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 27 citations in OpenAlex.
- Repairing the defective folding of alpha-sarcoglycan is needed to promote myogenic cell engraftment in 3D artificial muscle models of LGMDR3.Skeletal muscle · 2025Article
- Pirfenidone treatment improves ischemic muscle function in mice with chronic kidney disease.Skeletal muscle · 2025Article
- Intramuscular adipose tissue restricts functional muscle recovery.Cell reports · 2025Article
- Deletion of the aryl hydrocarbon receptor in endothelial cells improves ischemic angiogenesis in chronic kidney disease.American journal of physiology. Heart and circulatory physiology · 2024Article
- IGF-1 Therapy Improves Muscle Size and Function in Experimental Peripheral Arterial Disease.JACC. Basic to translational science · 2023Article
- Eccentric contraction-induced strength loss in dystrophin-deficient muscle: Preparations, protocols, and mechanisms.The Journal of general physiology · 2023Article
- The 2022 On-site Padua Days on Muscle and Mobility Medicine hosts the University of Florida Institute of Myology and the Wellstone Center, March 30 - April 3, 2022 at the University of Padua and Thermae of Euganean Hills, Padua, Italy: The collection of abstracts.European journal of translational myology · 2022Article
- Supervillin Contributes to LPS-induced Inflammatory Response in THP-1 Cell-derived Macrophages.Inflammation · 2022Article
- Novel γ-sarcoglycan interactors in murine muscle membranes.Skeletal muscle · 2022Article
- Neuromuscular disease: 2021 update.Free neuropathology · 2021Article
- Effect of serotonin modulation on dystrophin-deficient zebrafish.Biology open · 2020Article
- Loss of supervillin causes myopathy with myofibrillar disorganization and autophagic vacuoles.Brain : a journal of neurology · 2020Article
- The ties that bind: functional clusters in limb-girdle muscular dystrophy.Skeletal muscle · 2020Review
- Generation and characterization of monoclonal antibodies that recognize human and murine supervillin protein isoforms.PloS one · 2018Article
- Preparation and Affinity-Purification of Supervillin Isoform 4 (SV4) Specific Polyclonal Antibodies.The protein journal · 2016Article
- Dystrophin-glycoprotein complex regulates muscle nitric oxide production through mechanoregulation of AMPK signaling.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Reengineering a transmembrane protein to treat muscular dystrophy using exon skipping.The Journal of clinical investigation · 2015Article
- Supervillin binds the Rac/Rho-GEF Trio and increases Trio-mediated Rac1 activation.Cytoskeleton (Hoboken, N.J.) · 2015Article
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Loss of gamma-sarcoglycan (γ-SG) induces muscle degeneration and signaling defects in response to mechanical load, and its absence is common to both Duchenne and limb girdle muscular dystrophies. Growing evidence suggests that aberrant signaling contributes to the disease pathology; however, the mechanisms of γ-SG-mediated mechanical signaling are poorly understood. To uncover γ-SG signaling pathway components, we performed yeast two-hybrid screens and identified the muscle-specific protein archvillin as a γ-SG and dystrophin interacting protein. Archvillin protein and message levels were significantly upregulated at the sarcolemma of murine γ-SG-null (gsg(-/-)) muscle but delocalized in dystrophin-deficient mdx muscle. Similar elevation of archvillin protein was observed in human quadriceps muscle lacking γ-SG. Reintroduction of γ-SG in gsg(-/-) muscle by rAAV injection restored archvillin levels to that of control C57 muscle. In situ eccentric contraction of tibialis anterior (TA) muscles from C57 mice caused ERK1/2 phosphorylation, nuclear activation of P-ERK1/2 and stimulus-dependent archvillin association with P-ERK1/2. In contrast, TA muscles from gsg(-/-) and mdx mice exhibited heightened P-ERK1/2 and increased nuclear P-ERK1/2 localization following eccentric contractions, but the archvillin-P-ERK1/2 association was completely ablated. These results position archvillin as a mechanically sensitive component of the dystrophin complex and demonstrate that signaling defects caused by loss of γ-SG occur both at the sarcolemma and in the nucleus.
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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.