ArticleEMBO reports2019
ATF7IP regulates SETDB1 nuclear localization and increases its ubiquitination.
Article in EMBO reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed, 78 citations in OpenAlex.
- Silencing the genome: role of HUSH complex in retrotransposon regulation and cancer development.Medical oncology (Northwood, London, England) · 2026Review
- ATF7ip Inhibits the Tumor Immune Response by Promoting Terminal CD8+ T-cell Exhaustion.Cancer immunology research · 2026Article
- HPL-2/HP1 and MET-2/SETDB1 bind distinct co-factors that promote heterochromatic foci, gene repression and organogenesis independently of H3K9 methylation.bioRxiv : the preprint server for biology · 2026Article
- Epigenetic lockdown of type I interferon sensing and signalling in human pluripotent cells.Nature communications · 2026Article
- The Many Faces of SetDB1.Epigenomes · 2026Review
- SETDB1/ATF7IP regulate the precise genome engineering of HUSH-regulated genes.Epigenetics & chromatin · 2026Article
- Cell density-dependent nuclear-cytoplasmic shuttling of SETDB1 integrates with Hippo signaling to regulate YAP1-mediated transcription.FEBS letters · 2026Article
- The Role of Histone Methyltransferase SETDB1 in Normal and Malignant Hematopoiesis.Cancer science · 2025Review
- MGA directly recruits SETDB1/ATF7IP for histone H3K9me3 mark on meiosis-related genes in mouse embryonic stem cells.iScience · 2025Article
- Ints7 deficiency activates DNA damage response to elicit resurgence of endogenous retrovirus MERVL and anastasis of embryonic stem cells.Nucleic acids research · 2025Article
- ATF7IP/SETDB1-mediated epigenetic programming regulates thymic homing and T lymphopoiesis of hematopoietic progenitors during embryogenesis.Nature communications · 2025Article
- The SUV39 Family of H3K9 Methyltransferases in Skeletal Muscle Stem Cells.FASEB bioAdvances · 2025Review
- Targeting SETDB1 in cancer and immune regulation: Potential therapeutic strategies in cancer.The Kaohsiung journal of medical sciences · 2025Review
- Stem cell activity-coupled suppression of endogenous retrovirus governs adult tissue regeneration.Cell · 2024Article
- SETDB1 activity is globally directed by H3K14 acetylation via its Triple Tudor Domain.Nucleic acids research · 2024Article
- Cell cycle length governs heterochromatin reprogramming during early development in non-mammalian vertebrates.EMBO reports · 2024Article
- Inheritance of H3K9 methylation regulates genome architecture in Drosophila early embryos.The EMBO journal · 2024Article
- SETDB1 deletion causes DNA demethylation and upregulation of multiple zinc-finger genes.Molecular biology reports · 2024Article
- SETDB1 as a cancer target: challenges and perspectives in drug design.RSC medicinal chemistry · 2024Review
- Cytoplasmic localization of SETDB1‑induced Warburg effect via c‑MYC‑LDHA axis enhances migration and invasion in breast carcinoma.International journal of molecular medicine · 2024Article
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Abstract
Understanding of the appropriate regulation of enzymatic activities of histone-modifying enzymes remains poor. The lysine methyltransferase, SETDB1, is one of the enzymes responsible for the methylation of histone H3 at lysine 9 (H3K9) and plays a key role in H3K9 trimethylation-mediated silencing of genes and retrotransposons. Here, we reported that how SETDB1's enzymatic activities can be regulated by the nuclear protein, ATF7IP, a known binding partner of SETDB1. Mechanistically, ATF7IP mediates SETDB1 retention inside the nucleus, presumably by inhibiting its nuclear export by binding to the N-terminal region of SETDB1, which harbors the nuclear export signal motifs, and also by promoting its nuclear import. The nuclear localization of SETDB1 increases its ubiquitinated, enzymatically more active form. Our results provided an insight as to how ATF7IP can regulate the histone methyltransferase activity of SETDB1 accompanied by its nuclear translocation.
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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.