ArticleRNA (New York, N.Y.)2003
Antagonistic regulation of alpha-actinin alternative splicing by CELF proteins and polypyrimidine tract binding protein.
Article in RNA (New York, N.Y.), 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
51 citing papers in PubMed, 105 citations in OpenAlex.
- CELF family of RNA-binding proteins: roles in disease biology and potential for therapeutic intervention.Cell communication and signaling : CCS · 2026Review
- Context base editing for splice correction of IVSI-110 β-thalassemia.Molecular therapy. Nucleic acids · 2024Article
- Bruno 1/CELF regulates splicing and cytoskeleton dynamics to ensure correct sarcomere assembly in Drosophila flight muscles.PLoS biology · 2024Article
- Integrative solution structure of PTBP1-IRES complex reveals strong compaction and ordering with residual conformational flexibility.Nature communications · 2023Article
- Clinical and Molecular Insights into Gastrointestinal Dysfunction in Myotonic Dystrophy Types 1 & 2.International journal of molecular sciences · 2022Review
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- A developmentally regulated spliced variant of PTBP1 is upregulated in type 1 diabetic hearts.Biochemical and biophysical research communications · 2019Article
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- The alternative splicing program of differentiated smooth muscle cells involves concerted non-productive splicing of post-transcriptional regulators.Nucleic acids research · 2016Article
- Splicing factors control C. elegans behavioural learning in a single neuron by producing DAF-2c receptor.Nature communications · 2016Article
- The lack of the Celf2a splicing factor converts a Duchenne genotype into a Becker phenotype.Nature communications · 2016Article
- RNA-binding proteins, neural development and the addictions.Genes, brain, and behavior · 2016Review
- Diverse regulation of 3' splice site usage.Cellular and molecular life sciences : CMLS · 2015Review
- Quaking and PTB control overlapping splicing regulatory networks during muscle cell differentiation.RNA (New York, N.Y.) · 2013Article
- 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
- Bcl-x pre-mRNA splicing regulates brain injury after neonatal hypoxia-ischemia.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- Ancient diversity of splicing motifs and protein surfaces in the wild emmer wheat (Triticum dicoccoides) LR10 coiled coil (CC) and leucine-rich repeat (LRR) domains.Molecular plant pathology · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
The alpha-actinin gene has a pair of alternatively spliced exons. The smooth muscle (SM) exon is repressed in most cell types by polypyrimidine tract binding protein (PTB). CELF (CUG-BP and ETR3-like factors) family proteins, splicing regulators whose activities are altered in myotonic dystrophy, were found to coordinately regulate selection of the two alpha-actinin exons. CUG-BP and ETR3 activated the SM exon, and along with CELF4 they were also able to repress splicing of the NM (nonmuscle) exon both in vivo and in vitro. Activation of SM exon splicing was associated with displacement of PTB from the polypyrimidine tract by binding of CUG-BP at adjacent sites. Our data provides direct evidence for the activity of CELF proteins as both activators and repressors of splicing within a single-model system of alternative splicing, and suggests a model whereby alpha-actinin alternative splicing is regulated by synergistic and antagonistic interactions between members of the CELF and PTB families.
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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.