ArticleMolecular and cellular biology2003
Alternative splicing controls myotonic dystrophy protein kinase structure, enzymatic activity, and subcellular localization.
Article in Molecular and cellular biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 62 citations in OpenAlex.
- Post-translational modification prediction via prompt-based fine-tuning of a GPT-2 model.Nature communications · 2024Article
- Nuclear Envelope Alterations in Myotonic Dystrophy Type 1 Patient-Derived Fibroblasts.International journal of molecular sciences · 2022Article
- Metabolic Alterations in Myotonic Dystrophy Type 1 and Their Correlation with Lipin.International journal of environmental research and public health · 2021Review
- Brain Pathogenesis and Potential Therapeutic Strategies in Myotonic Dystrophy Type 1.Frontiers in aging neuroscience · 2021Review
- AON-induced splice-switching and DMPK pre-mRNA degradation as potential therapeutic approaches for Myotonic Dystrophy type 1.Nucleic acids research · 2020Article
- DMPK is a New Candidate Mediator of Tumor Suppressor p53-Dependent Cell Death.Molecules (Basel, Switzerland) · 2019Article
- Expanded CUG repeats inRNA (New York, N.Y.) · 2019Article
- Insulin Signaling as a Key Moderator in Myotonic Dystrophy Type 1.Frontiers in neurology · 2019Review
- Abnormalities in Skeletal Muscle Myogenesis, Growth, and Regeneration in Myotonic Dystrophy.Frontiers in neurology · 2018Review
- In vivo assessment of muscle membrane properties in myotonic dystrophy.Muscle & nerve · 2016Article
- Genome Therapy of Myotonic Dystrophy Type 1 iPS Cells for Development of Autologous Stem Cell Therapy.Molecular therapy : the journal of the American Society of Gene Therapy · 2016Article
- Genome modification leads to phenotype reversal in human myotonic dystrophy type 1 induced pluripotent stem cell-derived neural stem cells.Stem cells (Dayton, Ohio) · 2015Article
- Myotonic dystrophy kinase-related Cdc42-binding kinases (MRCK), the ROCK-like effectors of Cdc42 and Rac1.Small GTPases · 2015Review
- Abnormal Lactate Levels Affect Motor Performance in Myotonic Dystrophy Type 1.European journal of translational myology · 2014Article
- 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
- Design and analysis of effects of triplet repeat oligonucleotides in cell models for myotonic dystrophy.Molecular therapy. Nucleic acids · 2013Article
- A tail-anchored myotonic dystrophy protein kinase isoform induces perinuclear clustering of mitochondria, autophagy, and apoptosis.PloS one · 2009Article
- Comparative transcriptional and biochemical studies in muscle of myotonic dystrophies (DM1 and DM2).Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2009Article
- Structure of dystrophia myotonica protein kinase.Protein science : a publication of the Protein Society · 2009Article
- Prediction of disease-related mutations affecting protein localization.BMC genomics · 2009Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transcripts of the myotonic dystrophy protein kinase (DMPK) gene, a member of the Rho kinase family, are subject to cell-type specific alternative splicing. An imbalance in the splice isoform profile of DMPK may play a role in the pathogenesis of DM1, a severe multisystemic disorder. Here, we report how structural subdomains determine biochemical properties and subcellular distribution of DMPK isoforms. A newly developed kinase assay revealed that DMPK is a Lys/Arg-directed kinase. Individual DMPK isoforms displayed comparable transphosphorylation activity and sequence preference for peptide substrates. However, DMPK autophosphorylation and phosphorylation of MYPT1 (as putative in vivo target of DMPK), were dependent on presence of an alternatively spliced VSGGG motif and the nature of the C terminus. In-gel effects of the VSGGG motif on the migration behavior of full-length kinase provide evidence for a model in which this motif mediates 3-D-conformational changes in DMPK isoforms. Finally, different C termini endow DMPK with the ability to bind to either endoplasmic reticulum or mitochondria or to adopt a cytosolic location. Our results suggest that DMPK isoforms have cell-type and location dependent substrate specificities with a role in organellar and cytoarchitectural dynamics.
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