ArticleProceedings of the National Academy of Sciences of the United States of America2015
The histone methyltransferase SETDB1 represses endogenous and exogenous retroviruses in B lymphocytes.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.
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Who cites it
75 citing papers in PubMed.
- Epigenetics in development, disease, and therapy: from mechanisms to clinical interventions.Science China. Life sciences · 2026Review
- LINE-1 Epigenetic Repression and Regulation of Immunity.Viruses · 2026Review
- Transposable Elements Are Dynamically Regulated in Medium Spiny Neurons and May Contribute to the Molecular and Behavioral Adaptations to Cocaine.Biological psychiatry · 2026Article
- The HIV-1 restriction factor RPRD2 does not inhibit transcription of HIV-1 or endogenous retroelements.bioRxiv : the preprint server for biology · 2026Article
- Transposable elements impact the human regulatory landscape through cell type specific epigenomic associations.Nature communications · 2026Article
- The Many Faces of SetDB1.Epigenomes · 2026Review
- Epigenetic mechanisms of retroviral regulation: a comparative review.Epigenetics & chromatin · 2026Review
- The expression, regulation, and function of human endogenous retroviruses in genitourinary cancers.Cell death discovery · 2025Review
- The Role of Histone Methyltransferase SETDB1 in Normal and Malignant Hematopoiesis.Cancer science · 2025Review
- Targeting SETDB1 in cancer and immune regulation: Potential therapeutic strategies in cancer.The Kaohsiung journal of medical sciences · 2025Review
- An integrated approach for the accurate detection of HERV-K HML-2 transcription and protein synthesis.Nucleic acids research · 2025Article
- Stem cell activity-coupled suppression of endogenous retrovirus governs adult tissue regeneration.Cell · 2024Article
- Histone methyltransferase SETDB1 safeguards mouse fetal hematopoiesis by suppressing activation of cryptic enhancers.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- A B cell screen against endogenous retroviruses identifies glycan-reactive IgM that recognizes a broad array of enveloped viruses.Science immunology · 2024Article
- The Roles of H3K9me3 Writers, Readers, and Erasers in Cancer Immunotherapy.International journal of molecular sciences · 2024Review
- GNAS knockout potentiates HDAC3 inhibition through viral mimicry-related interferon responses in lymphoma.Leukemia · 2024Article
- Lysine methylation modifications in tumor immunomodulation and immunotherapy: regulatory mechanisms and perspectives.Biomarker research · 2024Review
- Comprehensive Identification and Characterization of HML-9 Group in Chimpanzee Genome.Viruses · 2024Article
- 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
- Activation of endogenous retroviruses and induction of viral mimicry by MEK1/2 inhibition in pancreatic cancer.Science advances · 2024Article
15 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Genome stability relies on epigenetic mechanisms that enforce repression of endogenous retroviruses (ERVs). Current evidence suggests that distinct chromatin-based mechanisms repress ERVs in cells of embryonic origin (histone methylation dominant) vs. more differentiated cells (DNA methylation dominant). However, the latter aspect of this model has not been tested. Remarkably, and in contrast to the prevailing model, we find that repressive histone methylation catalyzed by the enzyme SETDB1 is critical for suppression of specific ERV families and exogenous retroviruses in committed B-lineage cells from adult mice. The profile of ERV activation in SETDB1-deficient B cells is distinct from that observed in corresponding embryonic tissues, despite the loss of repressive chromatin modifications at all ERVs. We provide evidence that, on loss of SETDB1, ERVs are activated in a lineage-specific manner depending on the set of transcription factors available to target proviral regulatory elements. These findings have important implications for genome stability in somatic cells, as well as the interface between epigenetic repression and viral latency.
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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.