ArticleMolecular neurobiology2012
The shortest isoform of dystrophin (Dp40) interacts with a group of presynaptic proteins to form a presumptive novel complex in the mouse brain.
Article in Molecular neurobiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 52 citations in OpenAlex.
- Mutation of leucine 170 alters the subcellular distribution, neurite outgrowth and three-dimensional structure of dystrophins Dp71 and Dp40.Molecular biology reports · 2026Article
- Genetic strategies for therapy of Duchenne muscular dystrophy.Molecular therapy. Nucleic acids · 2025Review
- Central Neurophysiological Alterations in Dystrophic mdx Mice Correlate With Reduced Hippocampal Levels of the Endogenous NMDA Receptor Ligand D-Aspartate.Journal of neurochemistry · 2025Article
- Deficient Astrocyte Homeostatic Support Contributes to Brain Impairment in Duchenne Muscular Dystrophy.Neurochemical research · 2025Review
- Characterization of Dystrophin Dp71 Expression and Interaction Partners in Embryonic Brain Development: Implications for Duchenne/Becker Muscular Dystrophy.Molecular neurobiology · 2025Article
- Advances in Duchenne Muscular Dystrophy: Diagnostic Techniques and Dystrophin Domain Insights.International journal of molecular sciences · 2025Review
- The role of dystrophin isoforms and interactors in the brain.Brain : a journal of neurology · 2025Review
- Learning, memory and blood-brain barrier pathology in Duchenne muscular dystrophy mice lacking Dp427, or Dp427 and Dp140.Genes, brain, and behavior · 2024Article
- Dystrophin- and Utrophin-Based Therapeutic Approaches for Treatment of Duchenne Muscular Dystrophy: A Comparative Review.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2024Review
- Nuclear Small Dystrophin Isoforms during Muscle Differentiation.Life (Basel, Switzerland) · 2023Article
- Ion Channels of the Sarcolemma and Intracellular Organelles in Duchenne Muscular Dystrophy: A Role in the Dysregulation of Ion Homeostasis and a Possible Target for Therapy.International journal of molecular sciences · 2023Review
- Startle responses in Duchenne muscular dystrophy: a novel biomarker of brain dystrophin deficiency.Brain : a journal of neurology · 2023Observational
- Dystrophin genetic variants and autism.Discover mental health · 2022Article
- Overexpression of the dystrophins Dp40 and Dp40Scientific reports · 2022Article
- Animal models for researching approaches to therapy of Duchenne muscular dystrophy.Transgenic research · 2021Review
- ε-Sarcoglycan: Unraveling the Myoclonus-Dystonia Gene.Molecular neurobiology · 2021Review
- Therapeutic aspects of cell signaling and communication in Duchenne muscular dystrophy.Cellular and molecular life sciences : CMLS · 2021Review
- Working Memory Alterations Plays an Essential Role in Developing Global Neuropsychological Impairment in Duchenne Muscular Dystrophy.Frontiers in psychology · 2020Article
- Schwann cell-specific Dp116 is expressed in glioblastoma cells, revealing two novelBiochemistry and biophysics reports · 2019Article
- Dystrophin is expressed in smooth muscle and afferent nerve fibers in the rat urinary bladder.Muscle & nerve · 2019Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Duchenne muscular dystrophy (DMD) causes cognitive impairment in one third of the patients, although the underlying mechanisms remain to be elucidated. Recent studies showed that mutations in the distal part of the dystrophin gene correlate well with the cognitive impairment in DMD patients, which is attributed to Dp71. The study on the expression of the shortest isoform, Dp40, has not been possible due to the lack of an isoform specific antibody. Dp40 has the same promoter as that found in Dp71 and lacks the normal C-terminal end of Dp427. In the present study, we have raised polyclonal antibody against the N-terminal sequence common to short isoforms of dystrophin, including Dp40, and investigated the expression pattern of Dp40 in the mouse brain. Affinity chromatography with this antibody and the consecutive LC-MS/MS analysis on the interacting proteins revealed that Dp40 was abundantly expressed in synaptic vesicles and interacted with a group of presynaptic proteins, including syntaxin1A and SNAP25, which are involved in exocytosis of synaptic vesicles in neurons. We thus suggest that Dp40 may form a novel protein complex and play a crucial role in presynaptic function. Further studies on these aspects of Dp40 function might provide more insight into the molecular mechanisms of cognitive impairment found in patients with DMD.
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