ArticleMolecular and cellular biology1992
Alternative splicing of a human alpha-tropomyosin muscle-specific exon: identification of determining sequences.
Article in Molecular and cellular biology, 1992. 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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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
26 citing papers in PubMed, 47 citations in OpenAlex.
- Tropomyosin 3 (TPM3) function in skeletal muscle and in myopathy.Skeletal muscle · 2023Review
- The mechanisms of a mammalian splicing enhancer.Nucleic acids research · 2018Article
- Diversification of the muscle proteome through alternative splicing.Skeletal muscle · 2018Review
- The conserved ubiquitin-like protein Hub1 plays a critical role in splicing in human cells.Journal of molecular cell biology · 2014Article
- Identification of splicing silencers and enhancers in sense Alus: a role for pseudoacceptors in splice site repression.Molecular and cellular biology · 2005Article
- Decrease in hnRNP A/B expression during erythropoiesis mediates a pre-mRNA splicing switch.The EMBO journal · 2002Article
- An exonic splicing silencer in the testes-specific DNA ligase III beta exon.Nucleic acids research · 2000Article
- Polypyrimidine tract binding protein functions as a repressor to regulate alternative splicing of alpha-actinin mutally exclusive exons.Molecular and cellular biology · 1999Article
- CA- and purine-rich elements form a novel bipartite exon enhancer which governs inclusion of the minute virus of mice NS2-specific exon in both singly and doubly spliced mRNAs.Molecular and cellular biology · 1999Article
- The role of evolutionarily conserved sequences in alternative splicing at the 3' end of Drosophila melanogaster myosin heavy chain RNA.Genetics · 1999Article
- hnRNP A1 recruited to an exon in vivo can function as an exon splicing silencer.Molecular and cellular biology · 1999Article
- Muscle-specific splicing of a heterologous exon mediated by a single muscle-specific splicing enhancer from the cardiac troponin T gene.Molecular and cellular biology · 1998Article
- An intronic sequence element mediates both activation and repression of rat fibroblast growth factor receptor 2 pre-mRNA splicing.Molecular and cellular biology · 1998Article
- Multiple interdependent sequence elements control splicing of a fibroblast growth factor receptor 2 alternative exon.Molecular and cellular biology · 1997Article
- The polypyrimidine tract binding protein binds upstream of neural cell-specific c-src exon N1 to repress the splicing of the intron downstream.Molecular and cellular biology · 1997Article
- Trans-acting factors regulate the expression of CD44 splice variants.The EMBO journal · 1996Article
- Muscle-specific splicing enhancers regulate inclusion of the cardiac troponin T alternative exon in embryonic skeletal muscle.Molecular and cellular biology · 1996Article
- A complex of nuclear proteins mediates SR protein binding to a purine-rich splicing enhancer.Proceedings of the National Academy of Sciences of the United States of America · 1996Article
- The exon sequence TAGG can inhibit splicing.Nucleic acids research · 1996Article
- Exon and intron sequences, respectively, repress and activate splicing of a fibroblast growth factor receptor 2 alternative exon.Molecular and cellular biology · 1995Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The human alpha-tropomyosin gene hTMnm has two mutually exclusive versions of exon 5 (NM and SK), one of which is expressed specifically in skeletal muscle (exon SK). A minigene construct expresses only the nonmuscle (NM) isoform when transfected into COS-1 cells and both forms when transfected into myoblasts. Twenty-four mutants were produced to determine why the SK exon is not expressed in COS cells. The results showed that exons NM and SK are not in competition for splicing to the flanking exons and that there is no intrinsic barrier to splicing between the exons. Instead, exon SK is skipped whenever there are flanking introns. Splicing of exon SK was induced when the branch site sequence 70 nucleotides upstream of the exon was mutated to resemble the consensus and when the extremities of the exon itself were changed to the corresponding NM sequence. Precise swaps of the NM and SK exon sequences showed that the exon sequence effect was dominant to that of intron sequences. The mechanism of regulation appears to be unlike that of other tropomyosin genes. We propose that exclusion of exon SK arises because its 3' splicing signals are weak and are prevented by an exon-specific repressor from competing for splice site recognition.
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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.