ArticleThe Journal of clinical investigation1997
Myotonic dystrophy protein kinase is involved in the modulation of the Ca2+ homeostasis in skeletal muscle cells.
Article in The Journal of clinical investigation, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 72 citations in OpenAlex.
- Skeletal muscle disorders as risk factors for type 2 diabetes.Molecular and cellular endocrinology · 2025Review
- Sex-specific sequels of early life stress on serine/threonine kinase activity in visceral adipose tissue from obese mice.bioRxiv : the preprint server for biology · 2024Article
- CaThe FEBS journal · 2022Article
- Molecular Therapies for Myotonic Dystrophy Type 1: From Small Drugs to Gene Editing.International journal of molecular sciences · 2022Review
- Genetic and Epigenetic Interplay Define Disease Onset and Severity in Repeat Diseases.Frontiers in aging neuroscience · 2022Review
- Dmpk gene deletion or antisense knockdown does not compromise cardiac or skeletal muscle function in mice.Human molecular genetics · 2016Article
- Can Human Pluripotent Stem Cell-Derived Cardiomyocytes Advance Understanding of Muscular Dystrophies?Journal of neuromuscular diseases · 2016Review
- In vivo assessment of muscle membrane properties in myotonic dystrophy.Muscle & nerve · 2016Article
- Epigenetics of the myotonic dystrophy-associated DMPK gene neighborhood.Epigenomics · 2016Article
- Muscle weakness in myotonic dystrophy associated with misregulated splicing and altered gating of Ca(V)1.1 calcium channel.Human molecular genetics · 2012Article
- A tail-anchored myotonic dystrophy protein kinase isoform induces perinuclear clustering of mitochondria, autophagy, and apoptosis.PloS one · 2009Article
- Correction of ClC-1 splicing eliminates chloride channelopathy and myotonia in mouse models of myotonic dystrophy.The Journal of clinical investigation · 2007Article
- Gene expression analysis in myotonic dystrophy: indications for a common molecular pathogenic pathway in DM1 and DM2.Gene expression · 2007Article
- Misregulation of alternative splicing causes pathogenesis in myotonic dystrophy.Progress in molecular and subcellular biology · 2006Review
- Environmental suppression of Neurospora crassa cot-1 hyperbranching: a link between COT1 kinase and stress sensing.Eukaryotic cell · 2003Article
- Alternative splicing controls myotonic dystrophy protein kinase structure, enzymatic activity, and subcellular localization.Molecular and cellular biology · 2003Article
- Expression profiling reveals altered satellite cell numbers and glycolytic enzyme transcription in nemaline myopathy muscle.Proceedings of the National Academy of Sciences of the United States of America · 2003Article
- Non-sarcolemmal muscular dystrophies.Brain pathology (Zurich, Switzerland) · 2001Review
- Differentiation markers of mouse C2C12 and rat L6 myogenic cell lines and the effect of the differentiation medium.In vitro cellular & developmental biology. Animal · 1999Article
- DMPK dosage alterations result in atrioventricular conduction abnormalities in a mouse myotonic dystrophy model.The Journal of clinical investigation · 1999Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myotonic dystrophy (DM), the most prevalent muscular disorder in adults, is caused by (CTG)n-repeat expansion in a gene encoding a protein kinase (DM protein kinase; DMPK) and involves changes in cytoarchitecture and ion homeostasis. To obtain clues to the normal biological role of DMPK in cellular ion homeostasis, we have compared the resting [Ca2+]i, the amplitude and shape of depolarization-induced Ca2+ transients, and the content of ATP-driven ion pumps in cultured skeletal muscle cells of wild-type and DMPK[-/-] knockout mice. In vitro-differentiated DMPK[-/-] myotubes exhibit a higher resting [Ca2+]i than do wild-type myotubes because of an altered open probability of voltage-dependent l-type Ca2+ and Na+ channels. The mutant myotubes exhibit smaller and slower Ca2+ responses upon triggering by acetylcholine or high external K+. In addition, we observed that these Ca2+ transients partially result from an influx of extracellular Ca2+ through the l-type Ca2+ channel. Neither the content nor the activity of Na+/K+ ATPase and sarcoplasmic reticulum Ca2+-ATPase are affected by DMPK absence. In conclusion, our data suggest that DMPK is involved in modulating the initial events of excitation-contraction coupling in skeletal muscle.
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