ArticleThe Journal of cell biology2021
ANO5 ensures trafficking of annexins in wounded myofibers.
Article in The Journal of cell biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.
What it found
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Who cites it
35 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.
- Sex differences in the involvement of skeletal and cardiac muscles in myopathicAmerican journal of physiology. Cell physiology · 2022Pooled it
- Distinct structural mechanisms drive gain-of-function activation of TMEM16E in gnathodiaphyseal dysplasia.Research square · 2026Article
- Sorcin couples Annexin A11 recruitment to ESCRT-III assembly for plasma membrane repair.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Sorcin couples Annexin A11 recruitment and ESCRT-III assembly during plasma membrane repair.bioRxiv : the preprint server for biology · 2026Article
- Tenascin-C from the tissue microenvironment promotes muscle stem cell maintenance and function through Annexin A2.Communications biology · 2025Article
- Cellular wound healing: A two-step mechanism of plasma membrane repair by annexins and calpains.The Journal of cell biology · 2025Article
- Calpains orchestrate secretion of annexin-containing microvesicles during membrane repair.The Journal of cell biology · 2025Article
- Revisiting the role of Annexins in membrane trafficking.Cellular and molecular life sciences : CMLS · 2025Review
- Anoctamin-5 deficiency enhances ATG9A-dependent autophagy, inducing osteogenesis and gnathodiaphyseal dysplasia-like bone formation.JCI insight · 2025Article
- Activation of TMEM16E scramblase induces ligand independent growth factor receptor signaling and macropinocytosis for membrane repair.Communications biology · 2025Article
- Muscular Dystrophies.Advances in experimental medicine and biology · 2025Review
- Mechanism of action and therapeutic value of anoctamin-1 in gastrointestinal cancers.Frontiers in immunology · 2025Review
- TMEM16 proteins: CaInternational journal of molecular medicine · 2024Review
- The tether function of the anoctamins.Cell calcium · 2024Review
- Annexins-a family of proteins with distinctive tastes for cell signaling and membrane dynamics.Nature communications · 2024Review
- Translational implications of targeting annexin A2: From membrane repair to muscular dystrophy, cardiovascular disease and cancer.Clinical and translational discovery · 2023Article
- Regulation of phospholipid distribution in the lipid bilayer by flippases and scramblases.Nature reviews. Molecular cell biology · 2023Review
- In vivo Electroporation of Skeletal Muscle Fibers in Mice.Bio-protocol · 2023Article
- TMEM16E regulates endothelial cell procoagulant activity and thrombosis.The Journal of clinical investigation · 2023Article
- AnnexinA6: a potential therapeutic target gene for extracellular matrix mineralization.Frontiers in cell and developmental biology · 2023Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Mutations in ANO5 (TMEM16E) cause limb-girdle muscular dystrophy R12. Defective plasma membrane repair is a likely mechanism. Using myofibers from Ano5 knockout mice, we show that trafficking of several annexin proteins, which together form a cap at the site of injury, is altered upon loss of ANO5. Annexin A2 accumulates at the wound to nearly twice the level observed in WT fibers, while annexin A6 accumulation is substantially inhibited in the absence of ANO5. Appearance of annexins A1 and A5 at the cap is likewise diminished in the Ano5 knockout. These changes are correlated with an alteration in annexin repair cap fine structure and shedding of annexin-positive vesicles. We conclude that loss of annexin coordination during repair is disrupted in Ano5 knockout mice and underlies the defective repair phenotype. Although ANO5 is a phospholipid scramblase, abnormal repair is rescued by overexpression of a scramblase-defective ANO5 mutant, suggesting a novel, scramblase-independent role of ANO5 in repair.
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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.