ArticleNature cell biology2013
SON connects the splicing-regulatory network with pluripotency in human embryonic stem cells.
Article in Nature cell biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.
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Who cites it
66 citing papers in PubMed.
- Targeting Osteoporosis-Osteoarthritis Comorbidity: Multi-Omics Identification of SON and Exploration of Therapeutic Agents.International journal of molecular sciences · 2026Article
- Small nucleolar RNA Snora61 drives self-renewal of intestinal stem cells via initiation of Lgr5 transcription.Nature communications · 2026Article
- NANOG Proximity Proteomics Maps Neighborhood Hubs Linked to Mesenchymal Stem Cell Stemness and Chromatin Control.Biomolecules · 2026Article
- U2AF2 controls alternative splicing in speckle-proximal regions in an RS domain-dependent manner.Nucleic acids research · 2026Article
- Biomolecular condensates in immune cell fate.Nature reviews. Immunology · 2025Review
- A systematic benchmark of Nanopore long-read RNA sequencing for transcript-level analysis in human cell lines.Nature methods · 2025Article
- RNA-binding protein SAMD4A targets FGF2 to regulate cardiomyocyte lineage specification from human embryonic stem cells.Stem cell research & therapy · 2025Article
- SON is an essential RNA splicing factor promoting ErbB2 and ErbB3 expression in breast cancer.British journal of cancer · 2024Article
- PRPF40A induces inclusion of exons in GC-rich regions important for human myeloid cell differentiation.Nucleic acids research · 2024Article
- SOX2 interacts with hnRNPK to modulate alternative splicing in mouse embryonic stem cells.Cell & bioscience · 2024Article
- Genome-wide Mapping of Topoisomerase Binding Sites Suggests Topoisomerase 3α (TOP3A) as a Reader of Transcription-Replication Conflicts (TRC).bioRxiv : the preprint server for biology · 2024Article
- Nuclear speckleopathies: developmental disorders caused by variants in genes encoding nuclear speckle proteins.Human genetics · 2024Review
- A mouse model of Zhu-Tokita-Takenouchi-Kim syndrome reveals indispensable SON functions in organ development and hematopoiesis.JCI insight · 2024Article
- A mouse model of ZTTK syndrome reveals indispensable SON functions in organ development and hematopoiesis.bioRxiv : the preprint server for biology · 2023Article
- Transcription factor E4F1 as a regulator of cell life and disease progression.Science advances · 2023Review
- Review
- RNA degradation eliminates developmental transcripts during murine embryonic stem cell differentiation via CAPRIN1-XRN2.Developmental cell · 2022Article
- A genotype-first analysis in a cohort of Mullerian anomaly.Journal of human genetics · 2022Article
- Establishing the phenotypic spectrum of ZTTK syndrome by analysis of 52 individuals with variants in SON.European journal of human genetics : EJHG · 2022Article
- CHERP Regulates the Alternative Splicing of pre-mRNAs in the Nucleus.International journal of molecular sciences · 2022Article
6 more citing papers are in PubMed but not listed here.
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9 authors.
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Abstract
Human embryonic stem cells (hESCs) harbour the ability to undergo lineage-specific differentiation into clinically relevant cell types. Transcription factors and epigenetic modifiers are known to play important roles in the maintenance of pluripotency of hESCs. However, little is known about regulation of pluripotency through splicing. In this study, we identify the spliceosome-associated factor SON as a factor essential for the maintenance of hESCs. Depletion of SON in hESCs results in the loss of pluripotency and cell death. Using genome-wide RNA profiling, we identified transcripts that are regulated by SON. Importantly, we confirmed that SON regulates the proper splicing of transcripts encoding for pluripotency regulators such as OCT4, PRDM14, E4F1 and MED24. Furthermore, we show that SON is bound to these transcripts in vivo. In summary, we connect a splicing-regulatory network for accurate transcript production to the maintenance of pluripotency and self-renewal of hESCs.
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