ArticleNucleic acids research2010
The neurofibromatosis type I pre-mRNA is a novel target of CELF protein-mediated splicing regulation.
Article in Nucleic acids research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 37 citations in OpenAlex.
- Expression Patterns of T-Cell Intracellular Antigen 1 in Neurodegenerative Disorders and Stroke.International journal of molecular sciences · 2026Review
- CELF1 Downregulation Promotes Cardiomyocyte Hypertrophy via Regulating Alternative Splicing of Tead1.Genes · 2026Article
- Neuron-specific repression of alternative splicing by the conserved CELF protein UNC-75 in Caenorhabditis elegans.Genetics · 2025Article
- Bibliometric Overview on T-Cell Intracellular Antigens and Their Pathological Implications.Biology · 2024Review
- CELF1 Selectively Regulates Alternative Splicing of DNA Repair Genes Associated With Cataract in Human Lens Cell Line.Biochemical genetics · 2023Article
- T-Cell Intracellular Antigen 1-Like Protein in Physiology and Pathology.International journal of molecular sciences · 2022Review
- Splicing is an alternate oncogenic pathway activation mechanism in glioma.Nature communications · 2022Article
- Distribution of alternative untranslated regions within the mRNA of the CELF1 splicing factor affects its expression.Scientific reports · 2022Article
- Using antisense oligonucleotides for the physiological modulation of the alternative splicing of NF1 exon 23a during PC12 neuronal differentiation.Scientific reports · 2021Article
- Nuclear Isoforms of Neurofibromin Are Required for Proper Spindle Organization and Chromosome Segregation.Cells · 2020Article
- CELF2 regulates the species-specific alternative splicing of TREM2.Scientific reports · 2020Article
- In vitro iCLIP-based modeling uncovers how the splicing factor U2AF2 relies on regulation by cofactors.Genome research · 2018Article
- Neurofibromatosis type 1 alternative splicing is a key regulator of Ras/ERK signaling and learning behaviors in mice.Human molecular genetics · 2017Article
- Article
- RNA helicase A activity is inhibited by oncogenic transcription factor EWS-FLI1.Nucleic acids research · 2015Article
- Neurofibromatosis type 1 alternative splicing is a key regulator of Ras signaling in neurons.Molecular and cellular biology · 2014Article
- CUG-BP, Elav-like family (CELF)-mediated alternative splicing regulation in the brain during health and disease.Molecular and cellular neurosciences · 2013Review
- Position-dependent and neuron-specific splicing regulation by the CELF family RNA-binding protein UNC-75 in Caenorhabditis elegans.Nucleic acids research · 2013Article
- CELF family RNA-binding protein UNC-75 regulates two sets of mutually exclusive exons of the unc-32 gene in neuron-specific manners in Caenorhabditis elegans.PLoS genetics · 2013Article
- Alternative splicing of the neurofibromatosis type 1 pre-mRNA is regulated by the muscleblind-like proteins and the CUG-BP and ELAV-like factors.BMC molecular biology · 2012Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The CUG-BP and ETR-3 like factors (CELF) are a family of six highly conserved RNA-binding proteins that preferentially bind to UG-rich sequences. One of the key functions of these proteins is to mediate alternative splicing in a number of tissues, including brain, heart and muscle. To fully understand the function of CELF proteins, it is important to identify downstream targets of CELF proteins. In this communication, we report that neurofibromatosis type I (NF1) exon 23a is a novel target of CELF protein-mediated splicing regulation in neuron-like cells. NF1 regulates Ras signaling, and the isoform that excludes exon 23a shows 10 times greater ability to down-regulate Ras signaling than the isoform that includes exon 23a. Five of the six CELF proteins strongly suppress the inclusion of NF1 exon 23a. Over-expression or siRNA knockdown of these proteins in cell transfection experiments altered the levels of NF1 exon 23a inclusion. In vitro binding and splicing analyses demonstrate that CELF proteins block splicing through interfering with binding of U2AF(65). These studies, combined with our previous investigations demonstrating a role for Hu proteins and TIA-1/TIAR in controlling NF1 exon 23a inclusion, highlight the complex nature of regulation of this important alternative splicing event.
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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.