ArticleNature communications2017
H3K14ac is linked to methylation of H3K9 by the triple Tudor domain of SETDB1.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed, 131 citations in OpenAlex.
- Dynamic regulation of H3K9 modifications in cancer: pathogenesis and targeted therapies.Biomarker research · 2026Review
- NRSF regulation of OPRM1 through histone acetylation.Clinical epigenetics · 2026Article
- Histone modification cross-talk: analytical tools and molecular mechanisms.The Biochemical journal · 2026Review
- The Many Faces of SetDB1.Epigenomes · 2026Review
- Ketogenic diet dampens excitatory neurotransmission by shrinking synaptic vesicle pools.Cell reports · 2026Article
- Histone 3 lysine 9 dimethylation by the G9a-GLP heterodimer requires intranucleosomal product reading.bioRxiv : the preprint server for biology · 2026Article
- Computational assessment of the relationship between metabolism and histone methylation in cancer cells.PloS one · 2026Article
- Synergistic regulation by H3K36 and H3K27 methylation defines the chromatin landscape to control virulence and secondary metabolism in a fungal pathogen.Genome research · 2025Article
- Antagonistic regulation of LINE-1/Alu elements and their repressor APOBEC3B in cellular senescence.Mobile DNA · 2025Article
- Mechanistic insights into the stimulation of the histone H3K9 methyltransferase Clr4 by proximal H3K14 ubiquitination.Science advances · 2025Article
- Potent and selective SETDB1 covalent negative allosteric modulator reduces methyltransferase activity in cells.Nature communications · 2025Article
- BRD1 deficiency affects SREBF1-related lipid metabolism through regulating H3K9ac/H3K9me3 transition to inhibit HCC progression.Cell death & disease · 2025Article
- A Target Class Ligandability Evaluation of WD40 Repeat-Containing Proteins.Journal of medicinal chemistry · 2025Article
- SETDB1 activity is globally directed by H3K14 acetylation via its Triple Tudor Domain.Nucleic acids research · 2024Article
- Distinct H3K9me3 heterochromatin maintenance dynamics govern different gene programmes and repeats in pluripotent cells.Nature cell biology · 2024Article
- Distinct H3K9me3 heterochromatin maintenance dynamics govern different gene programs and repeats in pluripotent cells.bioRxiv : the preprint server for biology · 2024Article
- H3K14ac facilitates the reinstallation of constitutive heterochromatin inProceedings of the National Academy of Sciences of the United States of America · 2024Article
- asteRIa enables robust interaction modeling between chromatin modifications and epigenetic readers.Nucleic acids research · 2024Article
- SETDB1 as a cancer target: challenges and perspectives in drug design.RSC medicinal chemistry · 2024Review
- One form and two functions: MBD of SETDB2 is a protein-interacting domain.Structure (London, England : 1993) · 2024Article
Corrections and comments
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Authors and funding
17 authors at 2 institutions in 3 countries.
Funding
Abstract
SETDB1 is an essential H3K9 methyltransferase involved in silencing of retroviruses and gene regulation. We show here that its triple Tudor domain (3TD) specifically binds to doubly modified histone H3 containing K14 acetylation and K9 methylation. Crystal structures of 3TD in complex with H3K14ac/K9me peptides reveal that peptide binding and K14ac recognition occurs at the interface between Tudor domains (TD) TD2 and TD3. Structural and biochemical data demonstrate a pocket switch mechanism in histone code reading, because K9me1 or K9me2 is preferentially recognized by the aromatic cage of TD3, while K9me3 selectively binds to TD2. Mutations in the K14ac/K9me binding sites change the sub-nuclear localization of 3TD. ChIP-seq analyses show that SETDB1 is enriched at H3K9me3 regions and K9me3/K14ac is enriched at SETDB1 binding sites overlapping with LINE elements, suggesting that recruitment of the SETDB1 complex to K14ac/K9me regions has a role in silencing of active genomic regions.
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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.