ArticleThe EMBO journal1994
Smooth muscle-specific switching of alpha-tropomyosin mutually exclusive exon selection by specific inhibition of the strong default exon.
Article in The EMBO journal, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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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
50 citing papers in PubMed, 101 citations in OpenAlex.
- MBNL loss of function in smooth muscle as a model for myotonic dystrophy associated gastrointestinal dysmotility.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Cell-type specific regulator RBPMS switches alternative splicing via higher-order oligomerization and heterotypic interactions with other splicing regulators.Nucleic acids research · 2023Article
- Myocardin regulates exon usage in smooth muscle cells through induction of splicing regulatory factors.Cellular and molecular life sciences : CMLS · 2022Article
- A drug-repositioning screen using splicing-sensitive fluorescent reporters identifies novel modulators of VEGF-A splicing with anti-angiogenic properties.Oncogenesis · 2021Article
- Article
- Programmable mutually exclusive alternative splicing for generating RNA and protein diversity.Nature communications · 2019Article
- The alternative splicing program of differentiated smooth muscle cells involves concerted non-productive splicing of post-transcriptional regulators.Nucleic acids research · 2016Article
- Diverse regulation of 3' splice site usage.Cellular and molecular life sciences : CMLS · 2015Review
- New insights into functional roles of the polypyrimidine tract-binding protein.International journal of molecular sciences · 2013Review
- Introducing a special edition of the Journal of Muscle Research and Cell Motility on tropomyosin: form and function.Journal of muscle research and cell motility · 2013Article
- MBNL1 and PTB cooperate to repress splicing of Tpm1 exon 3.Nucleic acids research · 2013Article
- Stoichiometry of a regulatory splicing complex revealed by single-molecule analyses.The EMBO journal · 2010Article
- iCLIP reveals the function of hnRNP particles in splicing at individual nucleotide resolution.Nature structural & molecular biology · 2010Article
- Four exons of the serotonin receptor 4 gene are associated with multiple distant branch points.RNA (New York, N.Y.) · 2010Article
- Modulating alternative splicing by cotranscriptional cleavage of nascent intronic RNA.RNA (New York, N.Y.) · 2008Article
- Activation of alpha-tropomyosin exon 2 is regulated by the SR protein 9G8 and heterogeneous nuclear ribonucleoproteins H and F.Molecular and cellular biology · 2006Article
- An apparent pseudo-exon acts both as an alternative exon that leads to nonsense-mediated decay and as a zero-length exon.Molecular and cellular biology · 2006Article
- A class of human exons with predicted distant branch points revealed by analysis of AG dinucleotide exclusion zones.Genome biology · 2006Article
- Exon selection in alpha-tropomyosin mRNA is regulated by the antagonistic action of RBM4 and PTB.Molecular and cellular biology · 2005Article
- Exon repression by polypyrimidine tract binding protein.RNA (New York, N.Y.) · 2005Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Exons 2 and 3 of alpha-tropomyosin are spliced in a strict mutually exclusive manner. Exon 3 is a default choice, being selected in almost all cell types where the gene is expressed. The default selection arises from a competition between the two exons, in which the stronger branch point/pyrimidine tract elements of exon 3 win. Exon 2 is selected predominantly or exclusively only in smooth muscle cells. We show here that the basis for the smooth muscle-specific switching of exon selection is inhibition of exon 3. Exon 3 is still skipped with smooth muscle specificity, even in the absence of exon 2. We have defined two conserved sequence elements, one in each of the introns flanking exon 3, that are essential for this regulation. Mutation of either element severely impairs regulated suppression of exon 3. No other exon or intron sequences appear to be necessary for regulation. We have also demonstrated skipping of exon 3 that is dependent upon both regulatory elements in an in vitro splicing assay. We further show that both splice sites of exon 3 must be inhibited in a concerted fashion to switch to selection of exon 2. This may relate to the requirement for negative elements on both sides of the exon.
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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.