ArticleJournal of muscle research and cell motility2000
Intracellular localization and isoform expression of the voltage-dependent anion channel (VDAC) in normal and dystrophic skeletal muscle.
Article in Journal of muscle research and cell motility, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 30 citations in OpenAlex.
- Mitochondrial‑endoplasmic reticulum crosstalk: Molecular mechanisms and implications for cardiovascular disease (Review).Molecular medicine reports · 2025Review
- Regulation of calcium homeostasis in endoplasmic reticulum-mitochondria crosstalk: implications for skeletal muscle atrophy.Cell communication and signaling : CCS · 2025Review
- Modulation of mitochondrial voltage dependent anion channel: studies on bilayer electrophysiology.Frontiers in physiology · 2025Review
- Differential Fatty Acid Response of Resident Macrophages in Human Skeletal Muscle Fiber and Intermuscular Adipose Tissue.International journal of molecular sciences · 2024Article
- Dietary oleic acid intake increases the proportion of type 1 and 2X muscle fibers in mice.Scientific reports · 2024Article
- Excitation-contraction coupling in mammalian skeletal muscle: Blending old and last-decade research.Frontiers in physiology · 2022Review
- Mitochondrial localization of PABPN1 in oculopharyngeal muscular dystrophy.Laboratory investigation; a journal of technical methods and pathology · 2019Article
- Expression of microRNAs and target proteins in skeletal muscle of rats selectively bred for high and low running capacity.American journal of physiology. Endocrinology and metabolism · 2017Article
- Tissue distribution of olive flounder VDAC2 and its expression in fish cell lines.Fish physiology and biochemistry · 2015Article
- Blockade of ActRIIB signaling triggers muscle fatigability and metabolic myopathy.Molecular therapy : the journal of the American Society of Gene Therapy · 2014Article
- Hepatoprotection through regulation of voltage dependent anion channel expression by Amomum subulatum Roxb seeds extract.Indian journal of pharmacology · 2011Article
- Myrica rubra Extracts Protect the Liver from CCl(4)-Induced Damage.Evidence-based complementary and alternative medicine : eCAM · 2011Article
- Inducible nitric oxide synthase is present in motor neuron mitochondria and Schwann cells and contributes to disease mechanisms in ALS mice.Brain structure & function · 2010Article
- Differential cerebral cortex transcriptomes of baboon neonates consuming moderate and high docosahexaenoic acid formulas.PloS one · 2007Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Voltage-dependent anion channels (VDACs) are a family of pore-forming proteins encoded by different genes, with at least three protein products expressed in mammalian tissues. The major recognized functional role of VDACs is to permit the almost free permeability of the outer mitochondrial membrane (OMM). Although VDAC1 is the best known among VDAC isoforms, its exclusively mitochondrial location is still debated. Therefore, we have measured its co-localization with markers of cellular organelles or compartments in skeletal muscle fibers by single or double immunofluorescence and traditional as well as confocal microscopy. Our results show that VDAC1 immunoreactivity corresponds to mitochondria and sarcoplasmic reticulum, while sarcolemmal reactivity, previously reported, was not observed. Since VDAC1 has been suggested to be involved in the control of oxidative phosphorylation, we sought for possible gene regulation of VDAC1, VDAC2 and VDAC3 in skeletal muscle of the dystrophin-deficient mdx mouse, which suffers of an impaired control of energy metabolism. Our results show that, while VDAC1 mRNA and protein and VDAC2 mRNA are normally expressed. VDAC3 mRNA is markedly down-regulated in mdx mouse muscle at different ages (before, during and after the outburst of myofiber necrosis). This finding suggests a possible involvement of VDAC3 expression in the early pathogenic events of the mdx muscular dystrophy.
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