ArticleJournal of muscle research and cell motility2011
Ahnak1 abnormally localizes in muscular dystrophies and contributes to muscle vesicle release.
Article in Journal of muscle research and cell motility, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 25 citations in OpenAlex.
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- Transcriptomic and proteomic profiling shows dysregulated immune and metabolic pathways in arrhythmogenic cardiomyopathy.ESC heart failure · 2025Article
- Comparative Analysis of Primary Sarcopenia and End-Stage Renal Disease-Related Muscle Wasting Using Multi-Omics Approaches.Journal of cachexia, sarcopenia and muscle · 2025Article
- Palmitoylation-dependent association with Annexin II directs hepatitis E virus ORF3 sorting into vesicles and quasi-enveloped virions.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
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- Deep whole-genome sequencing of multiple proband tissues and parental blood reveals the complex genetic etiology of congenital diaphragmatic hernias.HGG advances · 2020Article
- The S100B Protein and Partners in Adipocyte Response to Cold Stress and Adaptive Thermogenesis: Facts, Hypotheses, and Perspectives.Biomolecules · 2020Review
- AHNAK2 Promotes Migration, Invasion, and Epithelial-Mesenchymal Transition in Lung Adenocarcinoma Cells via the TGF-β/Smad3 Pathway.OncoTargets and therapy · 2020Article
- Electrical stimulation increases hypertrophy and metabolic flux in tissue-engineered human skeletal muscle.Biomaterials · 2019Article
- Tmem2 regulates cell-matrix interactions that are essential for muscle fiber attachment.Development (Cambridge, England) · 2016Article
- AHNAK enables mammary carcinoma cells to produce extracellular vesicles that increase neighboring fibroblast cell motility.Oncotarget · 2016Article
- GRAF1 deficiency blunts sarcolemmal injury repair and exacerbates cardiac and skeletal muscle pathology in dystrophin-deficient mice.Skeletal muscle · 2015Article
- Periaxin and AHNAK nucleoprotein 2 form intertwined homodimers through domain swapping.The Journal of biological chemistry · 2014Article
- Defects in glycosylation impair satellite stem cell function and niche composition in the muscles of the dystrophic Large(myd) mouse.Stem cells (Dayton, Ohio) · 2012Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ahnak1 is a giant, ubiquitously expressed, plasma membrane support protein whose function in skeletal muscle is largely unknown. Therefore, we investigated whether ahnak would be influenced by alterations of the sarcolemma exemplified by dysferlin mutations known to render the sarcolemma vulnerable or by mutations in calpain3, a protease known to cleave ahnak. Human muscle biopsy specimens obtained from patients with limb girdle muscular dystrophy (LGMD) caused by mutations in dysferlin (LGMD2B) and calpain3 (LGMD2A) were investigated for ahnak expression and localization. We found that ahnak1 has lost its sarcolemmal localization in LGMD2B but not in LGMD2A. Instead ahnak1 appeared in muscle connective tissue surrounding the extracellular site of the muscle fiber in both muscular dystrophies. The entire giant ahnak1 molecule was present outside the muscle fiber and did only partially colocalize with CD45-positive immune cell infiltration and the extracelluar matrix proteins fibronectin and collagenVI. Further, vesicles shedded in response to Ca(2+) by primary human myotubes were purified and their protein content was analysed. Ahnak1 was prominently present in these vesicles. Electron microscopy revealed a homogenous population of vesicles with a diameter of about 150 nm. This is the first study demonstrating vesicle release from human myotubes that may be one mechanism underlying abnormally localized ahnak1. Taken together, our results define ahnak1 in muscle connective tissue as a novel feature of two genetically distinct muscular dystrophies that might contribute to disease pathology.
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