ArticleThe EMBO journal1999
Modulation of exon skipping by high-affinity hnRNP A1-binding sites and by intron elements that repress splice site utilization.
Article in The EMBO journal, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 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
93 citing papers in PubMed, 200 citations in OpenAlex.
- Inverted Alu repeats in loop-out exon skipping across hominoid evolution.Nucleic acids research · 2026Article
- The differential impact of HNRNPA1 isoforms on gene expression and their relevance to dsRNA-mediated innate immune response.Scientific reports · 2025Article
- Potential and Optimization of Mammalian Splice Riboswitches for the Regulation of Exon Skipping-Dependent Gene Expression and Isoform Switching within theACS synthetic biology · 2025Article
- Truncated SCRIB isoform promotes breast cancer metastasis through HNRNP A1 mediated exon 16 skipping.Acta pharmacologica Sinica · 2023Article
- RNA in situ conformation sequencing reveals novel long-range RNA structures with impact on splicing.RNA (New York, N.Y.) · 2023Article
- RNA modifications in cardiovascular health and disease.Nature reviews. Cardiology · 2023Review
- Antisense Oligonucleotide Induction of the hnRNPA1b Isoform Affects Pre-mRNA Splicing ofInternational journal of molecular sciences · 2022Article
- Alternative Splicing in Human Biology and Disease.Methods in molecular biology (Clifton, N.J.) · 2022Article
- HNRNPM controls circRNA biogenesis and splicing fidelity to sustain cancer cell fitness.eLife · 2021Article
- Splicing at the phase-separated nuclear speckle interface: a model.Nucleic acids research · 2021Review
- Alternative splicing: Human disease and quantitative analysis from high-throughput sequencing.Computational and structural biotechnology journal · 2021Review
- TDP-43 regulates the alternative splicing of hnRNP A1 to yield an aggregation-prone variant in amyotrophic lateral sclerosis.Brain : a journal of neurology · 2018Article
- HNRNPA1 promotes recognition of splice site decoys by U2AF2 in vivo.Genome research · 2018Article
- Novel Pathological Role of hnRNPA1 (Heterogeneous Nuclear Ribonucleoprotein A1) in Vascular Smooth Muscle Cell Function and Neointima Hyperplasia.Arteriosclerosis, thrombosis, and vascular biology · 2017Article
- Genetic mutations in RNA-binding proteins and their roles in ALS.Human genetics · 2017Review
- Article
- An Ultraconserved Element (UCE) controls homeostatic splicing of ARGLU1 mRNA.Nucleic acids research · 2017Article
- Neuronal ELAVL proteins utilize AUF-1 as a co-partner to induce neuron-specific alternative splicing of APP.Scientific reports · 2017Article
- Global identification of hnRNP A1 binding sites for SSO-based splicing modulation.BMC biology · 2016Article
- Diverse regulation of 3' splice site usage.Cellular and molecular life sciences : CMLS · 2015Review
33 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
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The RNA-binding protein hnRNP A1 is a splicing regulator produced by exclusion of alternative exon 7B from the A1 pre-mRNA. Each intron flanking exon 7B contains a high-affinity A1-binding site. The A1-binding elements promote exon skipping in vivo, activate distal 5' splice site selection in vitro and improve the responsiveness of pre-mRNAs to increases in the concentration of A1. Whereas the glycine-rich C-terminal domain of A1 is not required for binding, it is essential to activate the distal 5' splice site. Because A1 complexes can interact simultaneously with two A1-binding sites, we propose that an interaction between bound A1 proteins facilitates the pairing of distant splice sites. Based on the distribution of putative A1-binding sites in various pre-mRNAs, an A1-mediated change in pre-mRNA conformation may help define the borders of mammalian introns. We also identify an intron element which represses the 3' splice site of exon 7B. The activity of this element is mediated by a factor distinct from A1. Our results suggest that exon 7B skipping results from the concerted action of several intron elements that modulate splice site recognition and pairing.
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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.