ArticleThe Journal of biological chemistry2011
Analysis of exonic regions involved in nuclear localization, splicing activity, and dimerization of Muscleblind-like-1 isoforms.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
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Who cites it
60 citing papers in PubMed, 80 citations in OpenAlex.
- Muscleblind-like proteins dimerize by forming disulfide bonds to regulate alternative splicing and pathogenic RNA foci formation.Nucleic acids research · 2026Article
- Muscleblind-like proteins dimerize by forming disulfide bonds to regulate alternative splicing and pathogenic RNA foci formation.bioRxiv : the preprint server for biology · 2026Article
- MBNL proteins in health, disease, and therapeutic applications.Nucleic acids research · 2026Review
- Targeting Expanded CUG and CTG Repeats as a Therapeutic Approach for Myotonic Dystrophy Type 1 (DM1).ChemMedChem · 2026Review
- MBNL1-mediated alternative splicing in cancer: underlying mechanism, isoform regulation, and translational perspectives.Frontiers in molecular biosciences · 2026Review
- Cardioprotective role of RBFox1 in myocardial infarction-induced heart failure.Cardiovascular research · 2025Article
- A Live-Cell NanoBRET Assay to Monitor RNA-Protein Interactions and Their Inhibition by Small Molecules.ACS central science · 2025Article
- circARHGAP10 as a candidate biomarker and therapeutic target in myotonic dystrophy type 1.Molecular therapy. Nucleic acids · 2025Article
- Article
- Functions of the Muscleblind-like protein family and their role in disease.Cell communication and signaling : CCS · 2025Review
- AntimiR treatment corrects myotonic dystrophy primary cell defects across several CTG repeat expansions with a dual mechanism of action.Science advances · 2024Article
- Alternative splicing in EMT and TGF-β signaling during cancer progression.Seminars in cancer biology · 2024Review
- ESRP1 controls biogenesis and function of a large abundant multiexon circRNA.Nucleic acids research · 2024Article
- FMRP deficiency leads to multifactorial dysregulation of splicing and mislocalization of MBNL1 to the cytoplasm.PLoS biology · 2023Article
- The Muscleblind-like protein MBL-1 regulates microRNA expression in Caenorhabditis elegans through an evolutionarily conserved autoregulatory mechanism.PLoS genetics · 2023Article
- Modulatory role of RNA helicases in MBNL-dependent alternative splicing regulation.Cellular and molecular life sciences : CMLS · 2023Article
- Muscleblind-1 interacts with tubulin mRNAs to regulate the microtubule cytoskeleton in C. elegans mechanosensory neurons.PLoS genetics · 2023Article
- Muscleblind-like proteins use modular domains to localize RNAs by riding kinesins and docking to membranes.Nature communications · 2023Article
- BlockmiR AONs as Site-Specific Therapeutic MBNL Modulation in Myotonic Dystrophy 2D and 3D Muscle Cells and HSAPharmaceutics · 2023Article
- How does precursor RNA structure influence RNA processing and gene expression?Bioscience reports · 2023Review
Corrections and comments
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Authors and funding
23 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Muscleblind-like-1 (MBNL1) is a splicing regulatory factor controlling the fetal-to-adult alternative splicing transitions during vertebrate muscle development. Its capture by nuclear CUG expansions is one major cause for type 1 myotonic dystrophy (DM1). Alternative splicing produces MBNL1 isoforms that differ by the presence or absence of the exonic regions 3, 5, and 7. To understand better their respective roles and the consequences of the deregulation of their expression in DM1, here we studied the respective roles of MBNL1 alternative and constitutive exons. By combining genetics, molecular and cellular approaches, we found that (i) the exon 5 and 6 regions are both needed to control the nuclear localization of MBNL1; (ii) the exon 3 region strongly enhances the affinity of MBNL1 for its pre-mRNA target sites; (iii) the exon 3 and 6 regions are both required for the splicing regulatory activity, and this function is not enhanced by an exclusive nuclear localization of MBNL1; and finally (iv) the exon 7 region enhances MBNL1-MBNL1 dimerization properties. Consequently, the abnormally high inclusion of the exon 5 and 7 regions in DM1 is expected to enhance the potential of MBNL1 of being sequestered with nuclear CUG expansions, which provides new insight into DM1 pathophysiology.
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