ArticleNature communications2021
A conserved role for the ALS-linked splicing factor SFPQ in repression of pathogenic cryptic last exons.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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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Who cites it
25 citing papers in PubMed, 32 citations in OpenAlex.
- CELF2 promotes 4R Tau splicing via nuclear clustering and drives cognitive dysfunction in tauopathy models.Nature communications · 2026Article
- SFPQ prevents MDA5-mediated activation of innate immunity and preserves cell viability.Cell reports · 2026Article
- SFPQ Promotes Homologous Recombination via mRNA Stabilization of RAD51 and Its Paralogs.Journal of molecular biology · 2026Article
- Protein oxidation in crowded environments.The Biochemical journal · 2026Review
- CELF2 Promotes Tau Exon 10 Inclusion via Hinge Domain-Mediated Nuclear Condensation, Driving Cognitive Dysfunction in Tauopathy Models.Research square · 2026Article
- TDP-43-mediated alternative polyadenylation is associated with a reduction in VPS35 and VPS29 expression in frontotemporal dementia.PLoS biology · 2026Article
- Single-nucleus transcriptome atlas of orbitofrontal cortex in ALS with a deep learning-based decoding of alternative polyadenylation mechanisms.Cell genomics · 2025Article
- TDP-43 nuclear loss in FTD/ALS causes widespread alternative polyadenylation changes.Nature neuroscience · 2025Article
- Enhanced hybridization-proximity labeling discovers protein interactomes of single RNA molecules.Nature communications · 2025Article
- SFPQ Promotes Homologous Recombination via mRNA Stabilization of RAD51 and Its Paralogs.bioRxiv : the preprint server for biology · 2025Article
- An alternative cytoplasmic SFPQ isoform with reduced phase separation potential is up-regulated in ALS.Science advances · 2025Article
- SFPQ subcellular mislocalisation entails altered cancer cell function.Clinical and translational medicine · 2025Article
- Live Imaging and Interactome Analysis of Zika and Chikungunya Viral RNAs Via Dual-Action Aptamer Tag.Research square · 2025Article
- Gene therapy breakthroughs in ALS: a beacon of hope for 20% of ALS patients.Translational neurodegeneration · 2025Review
- Emerging regulatory mechanisms and functions of biomolecular condensates: implications for therapeutic targets.Signal transduction and targeted therapy · 2025Review
- Virus-modified paraspeckle-like condensates are hubs for viral RNA processing and their formation drives genomic instability.Nature communications · 2024Article
- CELF2 promotes tau exon 10 inclusion via hinge domain-mediated nuclear condensation.bioRxiv : the preprint server for biology · 2024Article
- BindCompare: a novel integrated protein-nucleic acid binding analysis platform.Bioinformatics (Oxford, England) · 2024Article
- Serum Splicing Factor Proline- and Glutamine-Rich Is a Diagnostic Marker for Non-Small-Cell Lung Cancer and Other Solid Cancers.International journal of molecular sciences · 2024Article
- TDP-43 nuclear loss in FTD/ALS causes widespread alternative polyadenylation changes.bioRxiv : the preprint server for biology · 2024Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The RNA-binding protein SFPQ plays an important role in neuronal development and has been associated with several neurodegenerative disorders, including amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD), and Alzheimer's disease. Here, we report that loss of sfpq leads to premature termination of multiple transcripts due to widespread activation of previously unannotated cryptic last exons (CLEs). These SFPQ-inhibited CLEs appear preferentially in long introns of genes with neuronal functions and can dampen gene expression outputs and/or give rise to short peptides interfering with the normal gene functions. We show that one such peptide encoded by the CLE-containing epha4b mRNA isoform is responsible for neurodevelopmental defects in the sfpq mutant. The uncovered CLE-repressive activity of SFPQ is conserved in mouse and human, and SFPQ-inhibited CLEs are found expressed across ALS iPSC-derived neurons. These results greatly expand our understanding of SFPQ function and uncover a gene regulation mechanism with wide relevance to human neuropathologies.
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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.