ArticleNucleic acids research2018
SRSF9 selectively represses ADAR2-mediated editing of brain-specific sites in primates.
Article in Nucleic acids research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 34 citations in OpenAlex.
- A dual role of EZH2 in regulating A-to-I RNA editing and mRNA stability through ADAR.Nature communications · 2026Article
- Unraveling ADAR-Mediated Protein Recoding: A Proteogenomic Exploration in Model Organisms and Human Pathology.International journal of molecular sciences · 2025Review
- ADARs: pleiotropy in function, versatility in application.Nucleic acids research · 2025Review
- LZTS2 methylation as a potential diagnostic and prognostic marker in LIHC and STAD: Evidence from bioinformatics and in vitro analyses.Scientific reports · 2025Article
- ADAR2-mediated Q/R editing of GluA2 in homeostatic synaptic plasticity.Science signaling · 2025Article
- Dysregulation of heterochromatin caused by genomic structural variants may be central to autism spectrum disorder.Frontiers in molecular neuroscience · 2025Article
- Distinct interactomes of ADAR1 nuclear and cytoplasmic protein isoforms and their responses to interferon induction.Nucleic acids research · 2024Article
- SRSF9 promotes cell proliferation and migration of glioblastoma through enhancing CDK1 expression.Journal of cancer research and clinical oncology · 2024Article
- Harnessing ADAR-Mediated Site-Specific RNA Editing in Immune-Related Disease: Prediction and Therapeutic Implications.International journal of molecular sciences · 2023Review
- ELL associated factor 2 is a potential diagnostic and prognostic indicator: evidence from the in silico and in vitro experiments.American journal of cancer research · 2023Article
- Recent Advances in Adenosine-to-Inosine RNA Editing in Cancer.Cancer treatment and research · 2023Review
- Multiomic Profiling Identified EGF Receptor Signaling as a Potential Inhibitor of Type I Interferon Response in Models of Oncolytic Therapy by Vesicular Stomatitis Virus.International journal of molecular sciences · 2022Article
- Interplay between A-to-I Editing and Splicing of RNA: A Potential Point of Application for Cancer Therapy.International journal of molecular sciences · 2022Review
- ADRAM is an experience-dependent long noncoding RNA that drives fear extinction through a direct interaction with the chaperone protein 14-3-3.Cell reports · 2022Article
- RNA editing of ion channels and receptors in physiology and neurological disorders.Oxford open neuroscience · 2022Review
- Pan-Cancer Analysis RevealedJournal of oncology · 2022Article
- Adenosine Deaminases Acting on RNA (ADARs) and Viral Infections.Annual review of virology · 2021Article
- Long Noncoding RNAInternational journal of molecular sciences · 2021Article
- SRSF9 Regulates Cassette Exon Splicing of Caspase-2 by Interacting with Its Downstream Exon.Cells · 2021Article
- Distant coupling between RNA editing and alternative splicing of the osmosensitive cation channel Tmem63b.The Journal of biological chemistry · 2020Article
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Adenosine-to-inosine (A-to-I) RNA editing displays diverse spatial patterns across different tissues. However, the human genome encodes only two catalytically active editing enzymes (ADAR1 and ADAR2), suggesting that other regulatory factors help shape the editing landscape. Here, we show that the splicing factor SRSF9 selectively controls the editing of many brain-specific sites in primates. SRSF9 is more lowly expressed in the brain than in non-brain tissues. Gene perturbation experiments and minigene analysis of candidate sites demonstrated that SRSF9 could robustly repress A-to-I editing by ADAR2. We found that SRSF9 biochemically interacted with ADAR2 in the nucleus via its RRM2 domain. This interaction required the presence of the RNA substrate and disrupted the formation of ADAR2 dimers. Transcriptome-wide location analysis and RNA sequencing revealed 1328 editing sites that are controlled directly by SRSF9. This regulon is significantly enriched for brain-specific sites. We further uncovered a novel motif in the ADAR2-dependent SRSF9 binding sites and provided evidence that the splicing factor prevents loss of cell viability by inhibiting ADAR2-mediated editing of genes involved in proteostasis, energy metabolism, the cell cycle and DNA repair. Collectively, our results highlight the importance of SRSF9 as an editing regulator and suggest potential roles for other splicing factors.
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