ArticleGenome research2015
Antagonistic regulation of mRNA expression and splicing by CELF and MBNL proteins.
Article in Genome research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 137 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
137 citing papers in PubMed, 1 synthesis or guideline pooled it, 188 citations in OpenAlex.
- Meta-Analysis of Multiple Sclerosis Microarray Data Reveals Dysregulation in RNA Splicing Regulatory Genes.International journal of molecular sciences · 2015Pooled it
- Overview on Epstein-Barr Virus-Host Interactions With a Focus on Host Cell Transcriptome Alterations.Cell biochemistry and function · 2026Review
- A Myocyte-Enriched Long Non-Coding RNA NRMLncR Enhances Myogenesis in Mouse.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Current biomarker development in myotonic dystrophies.Journal of neurology · 2026Review
- MBNL proteins in health, disease, and therapeutic applications.Nucleic acids research · 2026Review
- Enhanced muscle uptake of chemically optimized miR-23b antisense oligonucleotides as lead compounds for myotonic dystrophy type 1.American journal of human genetics · 2026Article
- Article
- Aberrant Splicing ofCirculation. Genomic and precision medicine · 2026Article
- CELF1 Downregulation Promotes Cardiomyocyte Hypertrophy via Regulating Alternative Splicing of Tead1.Genes · 2026Article
- MBNL1-mediated alternative splicing in cancer: underlying mechanism, isoform regulation, and translational perspectives.Frontiers in molecular biosciences · 2026Review
- Myotonic dystrophy type 1: clinical diversity, molecular insights and therapeutic perspectives.Nature reviews. Neurology · 2025Review
- Alternative splicing in stem cells and development: research progress and emerging technologies.Cell regeneration (London, England) · 2025Review
- Multisystem Symptoms in Myotonic Dystrophy Type 1: A Management and Therapeutic Perspective.International journal of molecular sciences · 2025Review
- Analysis of human urinary extracellular vesicles reveals disordered renal metabolism in myotonic dystrophy type 1.Nature communications · 2025Article
- RNA binding proteins (RBPs) on genetic stability and diseases.Global medical genetics · 2025Review
- Expression profile, regulatory mechanism and prognostic potential of MBNL2 in esophageal squamous cell carcinoma.Translational cancer research · 2025Article
- Functions of the Muscleblind-like protein family and their role in disease.Cell communication and signaling : CCS · 2025Review
- Review
- The Spatial-Temporal Alternative Splicing Profile Reveals the Functional Diversity of FXR1 Isoforms in Myogenesis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Decoding protein-RNA interactions using CLIP-based methodologies.Nature reviews. Genetics · 2024Review
77 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
RNA binding proteins of the conserved CUGBP1, Elav-like factor (CELF) family contribute to heart and skeletal muscle development and are implicated in myotonic dystrophy (DM). To understand their genome-wide functions, we analyzed the transcriptome dynamics following induction of CELF1 or CELF2 in adult mouse heart and of CELF1 in muscle by RNA-seq, complemented by crosslinking/immunoprecipitation-sequencing (CLIP-seq) analysis of mouse cells and tissues to distinguish direct from indirect regulatory targets. We identified hundreds of mRNAs bound in their 3' UTRs by both CELF1 and the developmentally induced MBNL1 protein, a threefold greater overlap in target messages than expected, including messages involved in development and cell differentiation. The extent of 3' UTR binding by CELF1 and MBNL1 predicted the degree of mRNA repression or stabilization, respectively, following CELF1 induction. However, CELF1's RNA binding specificity in vitro was not detectably altered by coincubation with recombinant MBNL1. These findings support a model in which CELF and MBNL proteins bind independently to mRNAs but functionally compete to specify down-regulation or localization/stabilization, respectively, of hundreds of mRNA targets. Expression of many alternative 3' UTR isoforms was altered following CELF1 induction, with 3' UTR binding associated with down-regulation of isoforms and genes. The splicing of hundreds of alternative exons was oppositely regulated by these proteins, confirming an additional layer of regulatory antagonism previously observed in a handful of cases. The regulatory relationships between CELFs and MBNLs in control of both mRNA abundance and splicing appear to have evolved to enhance developmental transitions in major classes of heart and muscle genes.
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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.