ArticleGenes & development1998
Identification of functional exonic splicing enhancer motifs recognized by individual SR proteins.
Article in Genes & development, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 237 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
237 citing papers in PubMed, 508 citations in OpenAlex.
- Circadian genes and risk of prostate cancer in the prostate cancer prevention trial.Molecular carcinogenesis · 2018Trial
- An in vivo parallelized reporter assay to uncover tissue-specific splicing regulatory sequences in a multicellular animal.Nucleic acids research · 2026Article
- U2AF1 modulates alternative exon selection and guards zygotic splicing activation in mouse preimplantation embryogenesis.Cellular and molecular life sciences : CMLS · 2026Article
- HSV ICP27 hijacks host splicing factor SRSF3 to regulate pre-mRNA splicing and export for viral gene expression and immune evasion.PLoS pathogens · 2026Article
- Phosphorylation-dependent regulation of serine/arginine-rich proteins and U2AF1 interactions in early spliceosome assembly.The Journal of biological chemistry · 2026Article
- Splice-switching ASOs targeting the AURKA 5' UTR collapse an SRSF1-AURKA-MYC oncogenic circuit in pancreatic cancer.Molecular cell · 2026Article
- DNA-damage dependent isoform switching modulates RIF1 DNA repair complex assembly and phase separation.The Journal of biological chemistry · 2025Article
- Massively parallel assay of human splice variants reveals cis-regulatory drivers of disease-associated and cell type-specific splicing regulation.bioRxiv : the preprint server for biology · 2025Article
- Deep indel mutagenesis reveals the regulatory and modulatory architecture of alternative exon splicing.Nature communications · 2025Article
- Non-viral intron knock-ins for targeted gene integration into human T cells and for T-cell selection.Nature biomedical engineering · 2025Article
- Complete omission of exon 21 from Slc12a2 transcripts in mice results in hearing loss.Scientific reports · 2025Article
- SRSF6 and SRSF1 coordinately enhance the inclusion of humanNAR molecular medicine · 2025Article
- The U1-70K and SRSF1 interaction is modulated by phosphorylation during the early stages of spliceosome assembly.Protein science : a publication of the Protein Society · 2024Article
- A second hotspot for pathogenic exon-skipping variants in CDC45.European journal of human genetics : EJHG · 2024Article
- Genetic and Clinical Analyses of theGenes · 2024Article
- SRSF1 is essential for primary follicle development by regulating granulosa cell survival via mRNA alternative splicing.Cellular and molecular life sciences : CMLS · 2023Article
- The rice blast fungus SR protein 1 regulates alternative splicing with unique mechanisms.PLoS pathogens · 2022Article
- SRSF6 balances mitochondrial-driven innate immune outcomes through alternative splicing of BAX.eLife · 2022Article
- Article
- Article
177 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Using an in vitro randomization and functional selection procedure, we have identified three novel classes of exonic splicing enhancers (ESEs) recognized by human SF2/ASF, SRp40, and SRp55, respectively. These ESEs are functional in splicing and are highly specific. For SF2/ASF and SRp55, in most cases, only the cognate SR protein can efficiently recognize an ESE and activate splicing. In contrast, the SRp40-selected ESEs can function with either SRp40 or SRp55, but not with SF2/ASF. UV cross-linking/competition and immunoprecipitation experiments showed that SR proteins recognize their cognate ESEs in nuclear extract by direct and specific binding. A motif search algorithm was used to derive consensus sequences for ESEs recognized by these SR proteins. Each SR protein yielded a distinct 5- to 7-nucleotide degenerate consensus. These three consensus sequences occur at higher frequencies in exons than in introns and may thus help define exon-intron boundaries. They occur in clusters within regions corresponding to naturally occurring, mapped ESEs. We conclude that a remarkably diverse set of sequences can function as ESEs. The degeneracy of these motifs is consistent with the fact that exonic enhancers evolved within extremely diverse protein coding sequences and are recognized by a small number of SR proteins that bind RNA with limited sequence specificity.
Indexed as
Identifiers
What OpenQuestion holds
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.