ArticlePloS one2009
A tail-anchored myotonic dystrophy protein kinase isoform induces perinuclear clustering of mitochondria, autophagy, and apoptosis.
Article in PloS one, 2009. 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, 27 citations in OpenAlex.
- Mitochondrial mechanisms in the pathogenesis of chronic inflammatory musculoskeletal disorders.Cell & bioscience · 2024Review
- Multi-level profiling unravels mitochondrial dysfunction in myotonic dystrophy type 2.Acta neuropathologica · 2024Article
- Mitochondrial Dysfunction in Repeat Expansion Diseases.Antioxidants (Basel, Switzerland) · 2023Review
- Resistance Exercise Training Rescues Mitochondrial Dysfunction in Skeletal Muscle of Patients with Myotonic Dystrophy Type 1.Journal of neuromuscular diseases · 2023Article
- Mitochondrial Dysfunction as an Underlying Cause of Skeletal Muscle Disorders.International journal of molecular sciences · 2022Review
- Senescence plays a role in myotonic dystrophy type 1.JCI insight · 2022Article
- Autophagy, Oxidative Stress and Cancer Development.Cancers · 2022Review
- Skeletal Muscle Mitochondria Dysfunction in Genetic Neuromuscular Disorders with Cardiac Phenotype.International journal of molecular sciences · 2021Review
- Oxidative Stress Triggers Defective Autophagy in Endothelial Cells: Role in Atherothrombosis Development.Antioxidants (Basel, Switzerland) · 2021Review
- Can long-term thiamine treatment improve the clinical outcomes of myotonic dystrophy type 1?Neural regeneration research · 2016Article
- Can Human Pluripotent Stem Cell-Derived Cardiomyocytes Advance Understanding of Muscular Dystrophies?Journal of neuromuscular diseases · 2016Review
- Oxidative stress and autophagy: the clash between damage and metabolic needs.Cell death and differentiation · 2015Review
- Muscle wasting in myotonic dystrophies: a model of premature aging.Frontiers in aging neuroscience · 2015Review
- Myotonic dystrophy protein kinase (DMPK) prevents ROS-induced cell death by assembling a hexokinase II-Src complex on the mitochondrial surface.Cell death & disease · 2013Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundStudies on the myotonic dystrophy protein kinase (DMPK) gene and gene products have thus far mainly concentrated on the fate of length mutation in the (CTG)n repeat at the DNA level and consequences of repeat expansion at the RNA level in DM1 patients and disease models. Surprisingly little is known about the function of DMPK protein products. METHODOLOGY/PRINCIPAL
findingsWe demonstrate here that transient expression of one major protein product of the human gene, the hDMPK A isoform with a long tail anchor, results in mitochondrial fragmentation and clustering in the perinuclear region. Clustering occurred in a variety of cell types and was enhanced by an intact tubulin cytoskeleton. In addition to morphomechanical changes, hDMPK A expression induces physiological changes like loss of mitochondrial membrane potential, increased autophagy activity, and leakage of cytochrome c from the mitochondrial intermembrane space accompanied by apoptosis. Truncation analysis using YFP-hDMPK A fusion constructs revealed that the protein's tail domain was necessary and sufficient to evoke mitochondrial clustering behavior. CONCLUSION/SIGNIFICANCE: Our data suggest that the expression level of the DMPK A isoform needs to be tightly controlled in cells where the hDMPK gene is expressed. We speculate that aberrant splice isoform expression might be a codetermining factor in manifestation of specific DM1 features in patients.
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