ArticleMuscle & nerve2021
hnRNP L is essential for myogenic differentiation and modulates myotonic dystrophy pathologies.
Article in Muscle & nerve, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 16 citations in OpenAlex.
- Disruption of RNA metabolism and its impact on protein homeostasis.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2026Review
- Transcriptome and Gene Family Analyses Reveal the Physiological and Immune Regulatory Mechanisms ofAntioxidants (Basel, Switzerland) · 2026Article
- The impact of Hnrnpl deficiency on transcriptional patterns of developing muscle cells.FEBS open bio · 2026Article
- The paradox of hnRNPK: both absence and excess impair skeletal muscle function in mice.Skeletal muscle · 2025Article
- The splicing factor hnRNPL demonstrates conserved myocardial regulation across species and is altered in heart failure.FEBS letters · 2024Article
- Epigenetic control of skeletal muscle atrophy.Cellular & molecular biology letters · 2024Review
- Research Progress on the Structural and Functional Roles of hnRNPs in Muscle Development.Biomolecules · 2023Review
- hnRNPL expression dynamics in the embryo and placenta.Gene expression patterns : GEP · 2023Article
- Calcitriol increases MBNL1 expression and alleviates myotonic dystrophy phenotypes in HSAJournal of translational medicine · 2022Article
- Enhanced myogenesis through lncFAM-mediated recruitment of HNRNPL to the MYBPC2 promoter.Nucleic acids research · 2022Article
- RNA-binding proteins modulate drug sensitivity of cancer cells.Emerging topics in life sciences · 2021Article
- RNA-Binding Proteins in the Post-transcriptional Control of Skeletal Muscle Development, Regeneration and Disease.Frontiers in cell and developmental biology · 2021Review
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Authors and funding
13 authors at 8 institutions in 2 countries.
Funding
Abstract
introductionRNA-binding proteins (RBPs) play an important role in skeletal muscle development and disease by regulating RNA splicing. In myotonic dystrophy type 1 (DM1), the RBP MBNL1 (muscleblind-like) is sequestered by toxic CUG repeats, leading to missplicing of MBNL1 targets. Mounting evidence from the literature has implicated other factors in the pathogenesis of DM1. Herein we sought to evaluate the functional role of the splicing factor hnRNP L in normal and DM1 muscle cells.
methodsCo-immunoprecipitation assays using hnRNPL and MBNL1 expression constructs and splicing profiling in normal and DM1 muscle cell lines were performed. Zebrafish morpholinos targeting hnrpl and hnrnpl2 were injected into one-cell zebrafish for developmental and muscle analysis. In human myoblasts downregulation of hnRNP L was achieved with shRNAi. Ascochlorin administration to DM1 myoblasts was performed and expression of the CUG repeats, DM1 splicing biomarkers, and hnRNP L expression levels were evaluated.
resultsUsing DM1 patient myoblast cell lines we observed the formation of abnormal hnRNP L nuclear foci within and outside the expanded CUG repeats, suggesting a role for this factor in DM1 pathology. We showed that the antiviral and antitumorigenic isoprenoid compound ascochlorin increased MBNL1 and hnRNP L expression levels. Drug treatment of DM1 muscle cells with ascochlorin partially rescued missplicing of established early biomarkers of DM1 and improved the defective myotube formation displayed by DM1 muscle cells. DISCUSSION: Together, these studies revealed that hnRNP L can modulate DM1 pathologies and is a potential therapeutic target.
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