ArticleNucleic acids research2017
Autoregulation of MBNL1 function by exon 1 exclusion from MBNL1 transcript.
Article in Nucleic acids research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 49 citations in OpenAlex.
- A chemoinformatics-guided platform for efficient discovery of RNA-binding small molecules: Proof-of-concept for myotonic dystrophy type 1.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
- A Live-Cell NanoBRET Assay to Monitor RNA-Protein Interactions and Their Inhibition by Small Molecules.ACS central science · 2025Article
- Promoter-targeted small RNA duplexes increase MBNL1 transcription and mitigate myotonic dystrophy-associated spliceopathy.Nucleic acids research · 2025Article
- Article
- Validation and in silico function prediction of circtial1 as a novel marker of abnormal lung development in nitrofen-induced congenital diaphragmatic hernia (CDH).Pediatric surgery international · 2024Article
- Article
- Alternative splicing and related RNA binding proteins in human health and disease.Signal transduction and targeted therapy · 2024Review
- Modulatory role of RNA helicases in MBNL-dependent alternative splicing regulation.Cellular and molecular life sciences : CMLS · 2023Article
- Sustainable recovery of MBNL activity in autoregulatory feedback loop in myotonic dystrophy.Molecular therapy. Nucleic acids · 2022Article
- Calcitriol increases MBNL1 expression and alleviates myotonic dystrophy phenotypes in HSAJournal of translational medicine · 2022Article
- Myotonic dystrophy RNA toxicity alters morphology, adhesion and migration of mouse and human astrocytes.Nature communications · 2022Article
- circMbl functions in cis and in trans to regulate gene expression and physiology in a tissue-specific fashion.Cell reports · 2022Article
- The X-linked splicing regulator MBNL3 has been co-opted to restrict placental growth in eutherians.PLoS biology · 2022Article
- A comprehensive atlas of fetal splicing patterns in the brain of adult myotonic dystrophy type 1 patients.NAR genomics and bioinformatics · 2022Article
- Distribution of alternative untranslated regions within the mRNA of the CELF1 splicing factor affects its expression.Scientific reports · 2022Article
- Preclinical characterization of antagomiR-218 as a potential treatment for myotonic dystrophy.Molecular therapy. Nucleic acids · 2021Article
- Cyclic mismatch binding ligands interact with disease-associated CGG trinucleotide repeats in RNA and suppress their translation.Nucleic acids research · 2021Article
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
Muscleblind-like proteins (MBNLs) are regulators of RNA metabolism. During tissue differentiation the level of MBNLs increases, while their functional insufficiency plays a crucial role in myotonic dystrophy (DM). Deep sequencing of RNA molecules cross-linked to immunoprecipitated protein particles (CLIP-seq) revealed that MBNL1 binds to MBNL1 exon 1 (e1) encoding both the major part of 5΄UTR and an amino-terminal region of MBNL1 protein. We tested several hypotheses regarding the possible autoregulatory function of MBNL1 binding to its own transcript. Our data indicate that MBNLs induce skipping of e1 from precursor MBNL1 mRNA and that e1 exclusion may impact transcript association with polysomes and translation. Furthermore, e1-deficient protein isoform lacking the first two zinc fingers is highly unstable and its EGFP fusion protein has severely compromised splicing activity. We also show that MBNL1 can be transcribed from three different promoters and that the transcription initiation site determines the mode of e1 regulation. Taken together, we demonstrate that MBNL proteins control steady-state levels of MBNL1 through an interaction with e1 in its precursor mRNA. Insights from our study open a new avenue in therapies against DM based on manipulation of the transcription initiation site and e1 splicing of MBNL1 mRNA.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.