ArticleHuman molecular genetics2016
Independent variability of microtubule perturbations associated with dystrophinopathy.
Article in Human molecular genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 55 citations in OpenAlex.
- Identification of myokines associated with the pathological stress response in theJournal of neuromuscular diseases · 2026Article
- C-terminal extension of HSPB6 in a family with myopathy and cataract.Human molecular genetics · 2026Article
- Embedding muscle fibers in hydrogel improves viability and preserves contractile function during prolonged ex vivo culture.The Journal of general physiology · 2026Article
- Bidirectional role of Costameres in the pathophysiology of mdx skeletal muscles.Human molecular genetics · 2025Article
- Stress exposure in the mdx mouse model of Duchenne muscular dystrophy provokes a widespread metabolic response.The FEBS journal · 2025Article
- Embedding muscle fibers in hydrogel improves viability and preserves contractile function during prolongedbioRxiv : the preprint server for biology · 2025Article
- Histone deacetylase 6 inhibition promotes microtubule acetylation and facilitates autophagosome-lysosome fusion in dystrophin-deficient mdx mice.Acta physiologica (Oxford, England) · 2025Article
- Review
- Acute microtubule changes linked to DMD pathology are insufficient to impair contractile function or enhance contraction-induced injury in healthy muscle.bioRxiv : the preprint server for biology · 2024Article
- Decreasing microtubule detyrosination modulates Nav1.5 subcellular distribution and restores sodium current in mdx cardiomyocytes.Cardiovascular research · 2024Article
- Retention of stress susceptibility in the mdx mouse model of Duchenne muscular dystrophy after PGC-1α overexpression or ablation of IDO1 or CD38.Human molecular genetics · 2024Article
- Dystrophin- and Utrophin-Based Therapeutic Approaches for Treatment of Duchenne Muscular Dystrophy: A Comparative Review.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2024Review
- IPSC derived cardiac fibroblasts of DMD patients show compromised actin microfilaments, metabolic shift and pro-fibrotic phenotype.Biology direct · 2023Article
- Eccentric contraction-induced strength loss in dystrophin-deficient muscle: Preparations, protocols, and mechanisms.The Journal of general physiology · 2023Article
- Evolution and developmental functions of the dystrophin-associated protein complex: beyond the idea of a muscle-specific cell adhesion complex.Frontiers in cell and developmental biology · 2023Review
- Promising therapeutic approaches of utrophin replacing dystrophin in the treatment of Duchenne muscular dystrophy.Fundamental research · 2022Review
- Tubulin acetylation increases cytoskeletal stiffness to regulate mechanotransduction in striated muscle.The Journal of general physiology · 2021Article
- Contraction-Induced Loss of Plasmalemmal Electrophysiological Function Is Dependent on the Dystrophin Glycoprotein Complex.Frontiers in physiology · 2021Article
- Rapid, redox-mediated mechanical susceptibility of the cortical microtubule lattice in skeletal muscle.Redox biology · 2020Article
- Social stress is lethal in the mdx model of Duchenne muscular dystrophy.EBioMedicine · 2020Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Absence of the protein dystrophin causes Duchenne muscular dystrophy. Dystrophin directly binds to microtubules in vitro, and its absence in vivo correlates with disorganization of the subsarcolemmal microtubule lattice, increased detyrosination of α-tubulin, and altered redox signaling. We previously demonstrated that the dystrophin homologue utrophin neither binds microtubules in vitro nor rescues microtubule lattice organization when overexpressed in muscles of dystrophin-deficient mdx mice. Here, we fine-mapped the dystrophin domain necessary for microtubule binding to spectrin-like repeats 20–22. We show that transgenic mdx mice expressing a full-length dystrophin/utrophin chimera completely lacking microtubule binding activity are surprisingly rescued for all measured dystrophic phenotypes, including full restoration of microtubule lattice organization. Conversely, despite the presence of dystrophin at the sarcolemma, β-sarcoglycan-deficient skeletal muscle presents with a disorganized and densified microtubule lattice. Finally, we show that the levels of α-tubulin detyrosination remain significantly elevated to that of mdx levels in transgenic mdx mice expressing nearly full-length dystrophin. Our results demonstrate that the microtubule-associated perturbations of mdx muscle are distinct, separable, and can vary independently from other parameters previously ascribed to dystrophin deficiency.
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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.