ArticleMolecular cell2016
SON and Its Alternatively Spliced Isoforms Control MLL Complex-Mediated H3K4me3 and Transcription of Leukemia-Associated Genes.
Article in Molecular cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 56 citations in OpenAlex.
- Toward unraveling molecular grammars for dsRNA-binding proteins: substrate recognition to binding mechanisms.BMB reports · 2025Review
- An Isoform-Specific RUNX1C-BTG2 Axis Governs AML Quiescence and Chemoresistance.Blood cancer discovery · 2025Article
- Major nuclear locales define nuclear genome organization and function beyond A and B compartments.eLife · 2025Article
- SON is an essential RNA splicing factor promoting ErbB2 and ErbB3 expression in breast cancer.British journal of cancer · 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
- miR-889-3p Facilitates the Browning Process of White Adipocyte Precursors by Targeting theInternational journal of molecular sciences · 2023Article
- SON is an essential mCell stem cell · 2023Article
- A mouse model of ZTTK syndrome reveals indispensable SON functions in organ development and hematopoiesis.bioRxiv : the preprint server for biology · 2023Article
- Article
- Distinctive Brain Malformations in Zhu-Tokita-Takenouchi-Kim Syndrome.AJNR. American journal of neuroradiology · 2022Article
- Establishing the phenotypic spectrum of ZTTK syndrome by analysis of 52 individuals with variants in SON.European journal of human genetics : EJHG · 2022Article
- FAK Activation Promotes SMC Dedifferentiation via Increased DNA Methylation in Contractile Genes.Circulation research · 2021Article
- ZTTK syndrome: Clinical and molecular findings of 15 cases and a review of the literature.American journal of medical genetics. Part A · 2021Article
- SON drives oncogenic RNA splicing in glioblastoma by regulating PTBP1/PTBP2 switching and RBFOX2 activity.Nature communications · 2021Article
- SON inhibits megakaryocytic differentiation via repressing RUNX1 and the megakaryocytic gene expression program in acute megakaryoblastic leukemia.Cancer gene therapy · 2021Article
- Focal Adhesion Kinase Activity and Localization is Critical for TNF-α-Induced Nuclear Factor-κB Activation.Inflammation · 2021Article
- son is necessary for proper vertebrate blood development.PloS one · 2021Article
- A de novo heterozygous variant in the SON gene is associated with Zhu-Tokita-Takenouchi-Kim syndrome.Molecular genetics & genomic medicine · 2020Article
- SON DNA-binding protein mediates macrophage autophagy and responses to intracellular infection.FEBS letters · 2020Article
Corrections and comments
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Authors and funding
14 authors at 5 institutions in 1 country.
Funding
Abstract
Dysregulation of MLL complex-mediated histone methylation plays a pivotal role in gene expression associated with diseases, but little is known about cellular factors modulating MLL complex activity. Here, we report that SON, previously known as an RNA splicing factor, controls MLL complex-mediated transcriptional initiation. SON binds to DNA near transcription start sites, interacts with menin, and inhibits MLL complex assembly, resulting in decreased H3K4me3 and transcriptional repression. Importantly, alternatively spliced short isoforms of SON are markedly upregulated in acute myeloid leukemia. The short isoforms compete with full-length SON for chromatin occupancy but lack the menin-binding ability, thereby antagonizing full-length SON function in transcriptional repression while not impairing full-length SON-mediated RNA splicing. Furthermore, overexpression of a short isoform of SON enhances replating potential of hematopoietic progenitors. Our findings define SON as a fine-tuner of the MLL-menin interaction and reveal short SON overexpression as a marker indicating aberrant transcriptional initiation in leukemia.
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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.