ArticleScientific reports2016
Negative autoregulation of BMP dependent transcription by SIN3B splicing reveals a role for RBM39.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 19 citations in OpenAlex.
- RNA splicing: Novel star in pulmonary diseases with a treatment perspective.Acta pharmaceutica Sinica. B · 2025Review
- Identification of hub genes and potential molecular mechanisms in MSS/MSI classifier primary colorectal cancer based on multiple datasets.Discover oncology · 2024Article
- Systematic pan-cancer analysis identifies RBM39 as an immunological and prognostic biomarker.Journal of cellular and molecular medicine · 2022Article
- Phosphoproteomic response of cardiac endothelial cells to ischemia and ultrasound.Biochimica et biophysica acta. Proteins and proteomics · 2021Article
- RNA-binding protein 39: a promising therapeutic target for cancer.Cell death discovery · 2021Review
- RBM39 Alters Phosphorylation of c-Jun and Binds to Viral RNA to Promote PRRSV Proliferation.Frontiers in immunology · 2021Article
- Article
- Genomics of rapid ecological divergence and parallel adaptation in four tidal marsh sparrows.Evolution letters · 2019Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
BMP signalling is negatively autoregulated by several genes including SMAD6, Noggin and Gremlin, and autoregulators are possible targets for enhancing BMP signalling in disorders such as fibrosis and pulmonary hypertension. To identify novel negative regulators of BMP signalling, we used siRNA screening in mouse C2C12 cells with a BMP-responsive luciferase reporter. Knockdown of several splicing factors increased BMP4-dependent transcription and target gene expression. Knockdown of RBM39 produced the greatest enhancement in BMP activity. Transcriptome-wide RNA sequencing identified a change in Sin3b exon usage after RBM39 knockdown. SIN3B targets histone deacetylases to chromatin to repress transcription. In mouse, Sin3b produces long and short isoforms, with the short isoform lacking the ability to recruit HDACs. BMP4 induced a shift in SIN3B expression to the long isoform, and this change in isoform ratio was prevented by RBM39 knockdown. Knockdown of long isoform SIN3B enhanced BMP4-dependent transcription, whereas knockdown of the short isoform did not. We propose that BMP4-dependent transcription is negatively autoregulated in part by SIN3B alternative splicing, and that RBM39 plays a role in this process.
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Registered trials
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