ArticleNucleic acids research2010
CELF proteins regulate CFTR pre-mRNA splicing: essential role of the divergent domain of ETR-3.
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 19 papers.
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Who cites it
19 citing papers in PubMed, 35 citations in OpenAlex.
- CELF2 promotes 4R Tau splicing via nuclear clustering and drives cognitive dysfunction in tauopathy models.Nature communications · 2026Article
- CELF family of RNA-binding proteins: roles in disease biology and potential for therapeutic intervention.Cell communication and signaling : CCS · 2026Review
- CELF2 Promotes Tau Exon 10 Inclusion via Hinge Domain-Mediated Nuclear Condensation, Driving Cognitive Dysfunction in Tauopathy Models.Research square · 2026Article
- tRNA-derived fragment tRF-24 drives CELF1 phase separation to promote oncogenic splicing in esophageal squamous cell carcinoma.Journal of experimental & clinical cancer research : CR · 2025Article
- Deep Intronic Mutation in SERPING1 Caused Hereditary Angioedema Through Pseudoexon Activation.Journal of clinical immunology · 2020Article
- RNA Binding Protein CELF2 Regulates Signal-Induced Alternative Polyadenylation by Competing with Enhancers of the Polyadenylation Machinery.Cell reports · 2019Article
- Alternative splicing regulation of doublesex gene by RNA-binding proteins in the silkworm Bombyx mori.RNA biology · 2019Article
- Aromatic side-chain conformational switch on the surface of the RNA Recognition Motif enables RNA discrimination.Nature communications · 2017Article
- Association of polymorphisms in genes of factors involved in regulation of splicing of cystic fibrosis transmembrane conductance regulator mRNA with acute respiratory distress syndrome in children with pneumonia.Critical care (London, England) · 2016Article
- Position-dependent activity of CELF2 in the regulation of splicing and implications for signal-responsive regulation in T cells.RNA biology · 2016Article
- Identification of Targets of CUG-BP, Elav-Like Family Member 1 (CELF1) Regulation in Embryonic Heart Muscle.PloS one · 2016Article
- Pre-mRNA splicing is facilitated by an optimal RNA polymerase II elongation rate.Genes & development · 2014Article
- Hu antigen R (HuR) is a positive regulator of the RNA-binding proteins TDP-43 and FUS/TLS: implications for amyotrophic lateral sclerosis.The Journal of biological chemistry · 2014Article
- Structural insights into the targeting of mRNA GU-rich elements by the three RRMs of CELF1.Nucleic acids research · 2013Article
- Position-dependent and neuron-specific splicing regulation by the CELF family RNA-binding protein UNC-75 in Caenorhabditis elegans.Nucleic acids research · 2013Article
- Alternative splicing: a pivotal step between eukaryotic transcription and translation.Nature reviews. Molecular cell biology · 2013Review
- Association of cystic fibrosis transmembrane conductance regulator gene variants with acute lung injury in African American children with pneumonia*.Critical care medicine · 2012Article
- CELFish ways to modulate mRNA decay.Biochimica et biophysica actaReview
- The importance of CELF control: molecular and biological roles of the CUG-BP, Elav-like family of RNA-binding proteins.Wiley interdisciplinary reviews. RNAReview
Corrections and comments
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Authors and funding
9 authors at 1 institution in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cystic fibrosis is a prominent genetic disease caused by mutations of the cystic fibrosis transmembrane conductance regulator (CFTR) gene. Among the many disease-causing alterations are pre-mRNA splicing defects that can hamper mandatory exon inclusion. CFTR exon 9 splicing depends in part on a polymorphic UG(m)U(n) sequence at the end of intron 8, which can be bound by TDP-43, leading to partial exon 9 skipping. CELF proteins, like CUG-BP1 and ETR-3, can also bind UG repeats and regulate splicing. We show here that ETR-3, but not CUG-BP1, strongly stimulates exon 9 skipping, although both proteins bind efficiently to the same RNA motif as TDP-43 and with higher affinity. We further show that the skipping of this exon may be due to the functional antagonism between U2AF65 and ETR-3 binding onto the polymorphic U or UG stretch, respectively. Importantly, we demonstrate that the divergent domain of ETR-3 is critical for CFTR exon 9 skipping, as shown by deletion and domain-swapping experiments. We propose a model whereby several RNA-binding events account for the complex regulation of CFTR exon 9 inclusion, with strikingly distinct activities of ETR-3 and CUG-BP1, related to the structure of their divergent domain.
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