ArticleBMC biology2016
Global identification of hnRNP A1 binding sites for SSO-based splicing modulation.
Article in BMC biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.
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Who cites it
43 citing papers in PubMed, 1 synthesis or guideline pooled it, 76 citations in OpenAlex.
- Decoding the role of aberrant RNA alternative splicing in hepatocellular carcinoma: a comprehensive review.Journal of cancer research and clinical oncology · 2023Pooled it
- Interpretable distillation reveals that deep learning splicing models suffer from pervasive confounders and blind spots.Genome biology · 2026Article
- hnRNPA1-SF3B3 interaction drives radioresistance in oral squamous cell carcinoma by modulating MARF1 alternative splicing isoforms.Journal of experimental & clinical cancer research : CR · 2026Article
- hnRNP A1 induces aberrantLife science alliance · 2025Article
- OCT4 translationally promotes AKT signaling as an RNA-binding protein in stressed pluripotent stem cells.Stem cell research & therapy · 2025Article
- Human hnRNPA1 reorganizes telomere-bound replication protein A.Nucleic acids research · 2024Article
- All exons are not created equal-exon vulnerability determines the effect of exonic mutations on splicing.Nucleic acids research · 2024Article
- RegulatingMolecular therapy. Nucleic acids · 2024Article
- hnRNP A1 dysfunction alters RNA splicing and drives neurodegeneration in multiple sclerosis (MS).Nature communications · 2024Article
- SINE-Associated LncRNA SAWPA Regulates Porcine Zygotic Genome Activation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Introme accurately predicts the impact of coding and noncoding variants on gene splicing, with clinical applications.Genome biology · 2023Article
- Structure and function analysis of Sam68 and hnRNP A1 synergy in the exclusion of exon 7 from SMN2 transcripts.Protein science : a publication of the Protein Society · 2023Article
- Prevalence, parameters, and pathogenic mechanisms for splice-altering acceptor variants that disrupt the AG exclusion zone.HGG advances · 2022Article
- Nuclear RNA binding regulates TDP-43 nuclear localization and passive nuclear export.Cell reports · 2022Article
- hnRNP A1 in RNA metabolism regulation and as a potential therapeutic target.Frontiers in pharmacology · 2022Review
- Alternative splicing of mRNA in colorectal cancer: new strategies for tumor diagnosis and treatment.Cell death & disease · 2021Review
- hnRNP A/B Proteins: An Encyclopedic Assessment of Their Roles in Homeostasis and Disease.Biology · 2021Review
- Let It Go: HIV-1Journal of virology · 2021Review
- A CRISPR RNA-binding protein screen reveals regulators of RUNX1 isoform generation.Blood advances · 2021Article
- Characterization of C9orf72 haplotypes to evaluate the effects of normal and pathological variations on its expression and splicing.PLoS genetics · 2021Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
Abstract
backgroundMany pathogenic genetic variants have been shown to disrupt mRNA splicing. Besides splice mutations in the well-conserved splice sites, mutations in splicing regulatory elements (SREs) may deregulate splicing and cause disease. A promising therapeutic approach is to compensate for this deregulation by blocking other SREs with splice-switching oligonucleotides (SSOs). However, the location and sequence of most SREs are not well known.
resultsHere, we used individual-nucleotide resolution crosslinking immunoprecipitation (iCLIP) to establish an in vivo binding map for the key splicing regulatory factor hnRNP A1 and to generate an hnRNP A1 consensus binding motif. We find that hnRNP A1 binding in proximal introns may be important for repressing exons. We show that inclusion of the alternative cassette exon 3 in SKA2 can be significantly increased by SSO-based treatment which blocks an iCLIP-identified hnRNP A1 binding site immediately downstream of the 5' splice site. Because pseudoexons are well suited as models for constitutive exons which have been inactivated by pathogenic mutations in SREs, we used a pseudoexon in MTRR as a model and showed that an iCLIP-identified hnRNP A1 binding site downstream of the 5' splice site can be blocked by SSOs to activate the exon.
conclusionsThe hnRNP A1 binding map can be used to identify potential targets for SSO-based therapy. Moreover, together with the hnRNP A1 consensus binding motif, the binding map may be used to predict whether disease-associated mutations and SNPs affect hnRNP A1 binding and eventually mRNA splicing.
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