ArticlePLoS currents2012
Repression of nuclear CELF activity can rescue CELF-regulated alternative splicing defects in skeletal muscle models of myotonic dystrophy.
Article in PLoS currents, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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Who cites it
14 citing papers in PubMed, 29 citations in OpenAlex.
- CELF family of RNA-binding proteins: roles in disease biology and potential for therapeutic intervention.Cell communication and signaling : CCS · 2026Review
- Cardiac Involvement in Myotonic Dystrophy Type 1: Mechanisms, Clinical Perspectives, and Emerging Therapeutic Strategies.International journal of molecular sciences · 2025Review
- Dissecting genomes of multiple yak populations: unveiling ancestry and high-altitude adaptation through whole-genome resequencing analysis.BMC genomics · 2025Article
- RNA binding proteins (RBPs) on genetic stability and diseases.Global medical genetics · 2025Review
- Caenorhabditis elegans ETR-1/CELF has broad effects on the muscle cell transcriptome, including genes that regulate translation and neuroblast migration.BMC genomics · 2022Article
- The Predicted RNA-Binding Protein ETR-1/CELF1 Acts in Muscles To Regulate Neuroblast Migration inG3 (Bethesda, Md.) · 2020Article
- Myotonic Dystrophy and Developmental Regulation of RNA Processing.Comprehensive Physiology · 2018Review
- Review
- CUG-BP, Elav-like family member 1 (CELF1) is required for normal myofibrillogenesis, morphogenesis, and contractile function in the embryonic heart.Developmental dynamics : an official publication of the American Association of Anatomists · 2016Article
- RNA-binding protein CELF1 promotes tumor growth and alters gene expression in oral squamous cell carcinoma.Oncotarget · 2015Article
- Evaluating the effects of CELF1 deficiency in a mouse model of RNA toxicity.Human molecular genetics · 2014Article
- RNA binding proteins in the regulation of heart development.The international journal of biochemistry & cell biology · 2013Review
- CUG-BP, Elav-like family (CELF)-mediated alternative splicing regulation in the brain during health and disease.Molecular and cellular neurosciences · 2013Review
- Smaug/SAMD4A restores translational activity of CUGBP1 and suppresses CUG-induced myopathy.PLoS genetics · 2013Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myotonic dystrophy type 1 (DM1) is caused by the expansion of CUG repeats in the 3' UTR of DMPK transcripts. DM1 pathogenesis has been attributed in part to alternative splicing dysregulation via elevation of CUG-BP, Elav-like family member 1 (CELF1). Several therapeutic approaches have been tested in cells and mice, but no previous studies had specifically targeted CELF1. Here, we show that repressing CELF activity rescues CELF-dependent alternative splicing in cell culture and transgenic mouse models of DM1. CELF-independent splicing, however, remained dysregulated. These data highlight both the potential and limitations of targeting CELF1 for the treatment of DM1.
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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.