ArticleScientific reports2017
Dynamin-2 mutations linked to Centronuclear Myopathy impair actin-dependent trafficking in muscle cells.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed.
- Beyond Membrane Remodeling: Organelle Crosstalk and Convergent Pathology in Centronuclear Myopathy.Muscles (Basel, Switzerland) · 2026Review
- Proteomic Analysis of Mouse Cerebral Cortex Following Experimental Ischemic Stroke: Identifying Novel Biomarkers of Damage and Repair.Cellular and molecular neurobiology · 2025Article
- Congenital myopathies: pathophysiological mechanisms and promising therapies.Journal of translational medicine · 2024Review
- GSK3α phosphorylates dynamin-2 to promote GLUT4 endocytosis in muscle cells.The Journal of cell biology · 2023Article
- The Long-Term Pannexin 1 Ablation Produces Structural and Functional Modifications in Hippocampal Neurons.Cells · 2022Article
- Gain-of-Function Dynamin-2 Mutations Linked to Centronuclear Myopathy Impair CaInternational journal of molecular sciences · 2022Article
- Article
- Centronuclear Myopathy Caused by Defective Membrane Remodelling of Dynamin 2 and BIN1 Variants.International journal of molecular sciences · 2022Review
- Gene deletion of γ-actin impairs insulin-stimulated skeletal muscle glucose uptake in growing mice but not in mature adult mice.Physiological reports · 2022Article
- Beta-Pix-dynamin 2 complex promotes colorectal cancer progression by facilitating membrane dynamics.Cellular oncology (Dordrecht, Netherlands) · 2021Article
- Common Pathogenic Mechanisms in Centronuclear and Myotubular Myopathies and Latest Treatment Advances.International journal of molecular sciences · 2021Review
- Dynamin Inhibitors Prevent the Establishment of the Cytomegalovirus Assembly Compartment in the Early Phase of Infection.Life (Basel, Switzerland) · 2021Article
- Panorama of the distal myopathies.Acta myologica : myopathies and cardiomyopathies : official journal of the Mediterranean Society of Myology · 2020Review
- Article
- Hyperglycemia impairs osteoblast cell migration and chemotaxis due to a decrease in mitochondrial biogenesis.Molecular and cellular biochemistry · 2020Article
- Lung Endothelial Transcytosis.Comprehensive Physiology · 2020Review
- Article
- Defects in G-Actin Incorporation into Filaments in Myoblasts Derived from Dysferlinopathy Patients Are Restored by Dysferlin C2 Domains.International journal of molecular sciences · 2019Article
- Metabolic regulation through the endosomal system.Traffic (Copenhagen, Denmark) · 2019Review
- Correlative SICM-FCM reveals changes in morphology and kinetics of endocytic pits induced by disease-associated mutations in dynamin.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
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Authors and funding
13 authors.
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Abstract
Dynamin-2 is a ubiquitously expressed GTP-ase that mediates membrane remodeling. Recent findings indicate that dynamin-2 also regulates actin dynamics. Mutations in dynamin-2 cause dominant centronuclear myopathy (CNM), a congenital myopathy characterized by progressive weakness and atrophy of skeletal muscles. However, the muscle-specific roles of dynamin-2 affected by these mutations remain elusive. Here we show that, in muscle cells, the GTP-ase activity of dynamin-2 is involved in de novo actin polymerization as well as in actin-mediated trafficking of the glucose transporter GLUT4. Expression of dynamin-2 constructs carrying CNM-linked mutations disrupted the formation of new actin filaments as well as the stimulus-induced translocation of GLUT4 to the plasma membrane. Similarly, mature muscle fibers isolated from heterozygous knock-in mice that harbor the dynamin-2 mutation p.R465W, an animal model of CNM, exhibited altered actin organization, reduced actin polymerization and impaired insulin-induced translocation of GLUT4 to the sarcolemma. Moreover, GLUT4 displayed aberrant perinuclear accumulation in biopsies from CNM patients carrying dynamin-2 mutations, further suggesting trafficking defects. These results suggest that dynamin-2 is a key regulator of actin dynamics and GLUT4 trafficking in muscle cells. Our findings also support a model in which impairment of actin-dependent trafficking contributes to the pathological mechanism in dynamin-2-associated CNM.
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