ArticleRNA (New York, N.Y.)1998
Enhancer elements activate the weak 3' splice site of alpha-tropomyosin exon 2.
Article in RNA (New York, N.Y.), 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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.
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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
17 citing papers in PubMed, 35 citations in OpenAlex.
- Nanopore sequencing reveals full-length Tropomyosin 1 isoforms and their regulation by RNA-binding proteins during rat heart development.Journal of cellular and molecular medicine · 2021Article
- Detection of polymorphism within leptin gene in Egyptian river buffalo and predict its effects on different molecular levels.Journal, genetic engineering & biotechnology · 2020Article
- Phosphorylation switches the general splicing repressor SRp38 to a sequence-specific activator.Nature structural & molecular biology · 2008Article
- Cross-kingdom patterns of alternative splicing and splice recognition.Genome biology · 2008Article
- Differing patterns of selection in alternative and constitutive splice sites.Genome research · 2007Article
- Interplay between exonic splicing enhancers, mRNA processing, and mRNA surveillance in the dystrophic Mdx mouse.PloS one · 2007Article
- 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
- The PTB interacting protein raver1 regulates alpha-tropomyosin alternative splicing.The EMBO journal · 2003Article
- Roles of hnRNP A1, SR proteins, and p68 helicase in c-H-ras alternative splicing regulation.Molecular and cellular biology · 2003Article
- PSF and p54nrb bind a conserved stem in U5 snRNA.RNA (New York, N.Y.) · 2002Article
- A splicing silencer that regulates smooth muscle specific alternative splicing is active in multiple cell types.Nucleic acids research · 2002Article
- RNA-protein interactions that regulate pre-mRNA splicing.Gene expression · 2002Review
- Article
- Identification and characterization of a novel serine-arginine-rich splicing regulatory protein.Molecular and cellular biology · 2000Article
- Identification of a bidirectional splicing enhancer: differential involvement of SR proteins in 5' or 3' splice site activation.Molecular and cellular biology · 1999Article
- Regulation of alternative RNA splicing by exon definition and exon sequences in viral and mammalian gene expression.Journal of biomedical scienceReview
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
We have identified four purine-rich sequences that act as splicing enhancer elements to activate the weak 3' splice site of alpha-tropomyosin exon 2. These elements also activate the splicing of heterologous substrates containing weak 3' splice sites or mutated 5' splice sites. However, they are unique in that they can activate splicing whether they are placed in an upstream or downstream exon, and the two central elements can function regardless of their position relative to one another. The presence of excess RNAs containing these enhancers could effectively inhibit in vitro pre-mRNA splicing reactions in a substrate-dependent manner and, at lower concentrations of competitor RNA, the addition of SR proteins could relieve the inhibition. However, when extracts were depleted by incubation with biotinylated exon 2 RNAs followed by passage over streptavidin agarose, SR proteins were not sufficient to restore splicing. Instead, both SR proteins and fractions containing a 110-kD protein were necessary to rescue splicing. Using gel mobility shift assays, we show that formation of stable enhancer-specific complexes on alpha-tropomyosin exon 2 requires the presence of both SR proteins and the 110-kD protein. By analogy to the doublesex exon enhancer elements in Drosophila, our results suggest that assembly of mammalian exon enhancer complexes requires both SR and non-SR proteins to activate selection of weak splice sites.
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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.