ArticlePloS one2017
SF3B1 is a stress-sensitive splicing factor that regulates both HSF1 concentration and activity.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 22 citations in OpenAlex.
- Human DEAH-box helicase 8 regulates HSF1-mediated stress response and cancer-associated pre-mRNA splicing in tumour cells.NAR cancer · 2026Article
- Activation of the heat shock response as a therapeutic strategy for tau toxicity.Disease models & mechanisms · 2024Article
- Spliceosome component Usp39 contributes to hepatic lipid homeostasis through the regulation of autophagy.Nature communications · 2023Article
- RNA splicing: a dual-edged sword for hepatocellular carcinoma.Medical oncology (Northwood, London, England) · 2022Review
- Highly dynamic transcriptional reprogramming and shorter isoform shifts under acute stresses during biological invasions.RNA biology · 2021Article
- Titration of SF3B1 Activity Reveals Distinct Effects on the Transcriptome and Cell Physiology.International journal of molecular sciences · 2020Article
- Article
- Negligible senescence in naked mole rats may be a consequence of well-maintained splicing regulation.GeroScience · 2020Article
- Changes in Proteome and Protein Phosphorylation Reveal the Protective Roles of Exogenous Nitrogen in Alleviating Cadmium Toxicity in Poplar Plants.International journal of molecular sciences · 2019Article
- Functional Network Analysis Reveals the Relevance of SKIIP in the Regulation of Alternative Splicing by p38 SAPK.Cell reports · 2019Article
- Article
- Alternative Splicing as a Target for Cancer Treatment.International journal of molecular sciences · 2018Review
- The heat-shock, or HSF1-mediated proteotoxic stress, response in cancer: from proteomic stability to oncogenesis.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2018Review
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Authors and funding
2 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
The heat shock response (HSR) is a well-conserved, cytoprotective stress response that activates the HSF1 transcription factor. During severe stress, cells inhibit mRNA splicing which also serves a cytoprotective function via inhibition of gene expression. Despite their functional interconnectedness, there have not been any previous reports of crosstalk between these two pathways. In a genetic screen, we identified SF3B1, a core component of the U2 snRNP subunit of the spliceosome, as a regulator of the heat shock response in Caenorhabditis elegans. Here, we show that this regulatory connection is conserved in cultured human cells and that there are at least two distinct pathways by which SF3B1 can regulate the HSR. First, inhibition of SF3B1 with moderate levels of Pladienolide B, a previously established small molecule inhibitor of SF3B1, affects the transcriptional activation of HSF1, the transcription factor that mediates the HSR. However, both higher levels of Pladienolide B and SF3B1 siRNA knockdown also change the concentration of HSF1, a form of HSR regulation that has not been previously documented during normal physiology but is observed in some forms of cancer. Intriguingly, mutations in SF3B1 have also been associated with several distinct types of cancer. Finally, we show that regulation of alternative splicing by SF3B1 is sensitive to temperature, providing a new mechanism by which temperature stress can remodel the transcriptome.
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