ArticlePLoS genetics2015
hnRNP K coordinates transcriptional silencing by SETDB1 in embryonic stem cells.
Article in PLoS genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 95 citations in OpenAlex.
- hnRNPK condensates facilitate enhancer-promoter looping and RNA polymerase II recruitment.Nature genetics · 2026Article
- Stable maintenance of MERVL-positive embryonic stem cells reveals sustained transcriptional programs and enhancer remodeling.The Journal of biological chemistry · 2026Article
- Stable Maintenance of Two-Cell-Like Cells from Embryonic Stem Cells Reveals Chromatin and Super Enhancer Regulation of MERVL Elements.bioRxiv : the preprint server for biology · 2025Article
- Mechanistic and Epigenetic Partitioning of Lamina-Associated Chromatin Revealed by a Genome-Wide Imaging Screen.bioRxiv : the preprint server for biology · 2025Article
- SOX2 interacts with hnRNPK to modulate alternative splicing in mouse embryonic stem cells.Cell & bioscience · 2024Article
- Evaluation of the RNA-dependence of PRC2 binding to chromatin in human pluripotent stem cells.bioRxiv : the preprint server for biology · 2024Article
- Exploring Transcriptional Regulation of Beta Cell SASP by Brd4-Associated Proteins and Cell Cycle Control Protein p21.Epigenomes · 2024Article
- Regulation of endogenous retroviruses in murine embryonic stem cells and early embryos.Journal of molecular cell biology · 2024Review
- The function of histone methyltransferase SETDB1 and its roles in liver cancer.Frontiers in cell and developmental biology · 2024Review
- Regulation of the heterochromatin spreading reaction byOpen biology · 2023Review
- The cytoplasmic fraction of the histone lysine methyltransferase Setdb1 is essential for embryonic stem cells.iScience · 2023Article
- Keratin 19 binds and regulates cytoplasmic HNRNPK mRNA targets in triple-negative breast cancer.BMC molecular and cell biology · 2023Article
- The Involvement of Ubiquitination and SUMOylation in Retroviruses Infection and Latency.Viruses · 2023Review
- Exploration of nuclear body-enhanced sumoylation reveals that PML represses 2-cell features of embryonic stem cells.Nature communications · 2022Article
- Review
- Deletion ofCells · 2022Article
- The regulation of totipotency transcription: Perspective fromFrontiers in cell and developmental biology · 2022Review
- Protein sumoylation in normal and cancer stem cells.Frontiers in molecular biosciences · 2022Review
- The Updating of Biological Functions of Methyltransferase SETDB1 and Its Relevance in Lung Cancer and Mesothelioma.International journal of molecular sciences · 2021Review
- Repeat to gene expression ratios in leukemic blast cells can stratify risk prediction in acute myeloid leukemia.BMC medical genomics · 2021Article
Corrections and comments
- Erratum issued
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Retrotransposition of endogenous retroviruses (ERVs) poses a substantial threat to genome stability. Transcriptional silencing of a subset of these parasitic elements in early mouse embryonic and germ cell development is dependent upon the lysine methyltransferase SETDB1, which deposits H3K9 trimethylation (H3K9me3) and the co-repressor KAP1, which binds SETDB1 when SUMOylated. Here we identified the transcription co-factor hnRNP K as a novel binding partner of the SETDB1/KAP1 complex in mouse embryonic stem cells (mESCs) and show that hnRNP K is required for ERV silencing. RNAi-mediated knockdown of hnRNP K led to depletion of H3K9me3 at ERVs, concomitant with de-repression of proviral reporter constructs and specific ERV subfamilies, as well as a cohort of germline-specific genes directly targeted by SETDB1. While hnRNP K recruitment to ERVs is dependent upon KAP1, SETDB1 binding at these elements requires hnRNP K. Furthermore, an intact SUMO conjugation pathway is necessary for SETDB1 recruitment to proviral chromatin and depletion of hnRNP K resulted in reduced SUMOylation at ERVs. Taken together, these findings reveal a novel regulatory hierarchy governing SETDB1 recruitment and in turn, transcriptional silencing in mESCs.
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Registered trials
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.