ArticleNature communications2018
A somatic role for the histone methyltransferase Setdb1 in endogenous retrovirus silencing.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.
What it found
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Who cites it
70 citing papers in PubMed, 107 citations in OpenAlex.
- Viral mimicry escape as a necessary feature of malignant transformation.Nature reviews. Cancer · 2026Review
- LINE-1 Epigenetic Repression and Regulation of Immunity.Viruses · 2026Review
- SETDB1 modulates neuroinflammation in the mouse cortex by regulating neuronal P2rx7 expression.Molecular psychiatry · 2026Article
- The Many Faces of SetDB1.Epigenomes · 2026Review
- Roles of TIF1β in Leukemic Stem Cell Through SETDB1-Dependent and Independent Mechanisms.Cancer science · 2026Review
- Loss of SETDB1-mediated H3K9me3 in human neural progenitor cells leads to transcriptional activation of L1 retrotransposons.Nucleic acids research · 2026Article
- Transposable Element Dysregulation in Hepatocellular Carcinoma: Epigenetic Mechanisms, Immune Remodeling, and Translational Opportunities.Journal of hepatocellular carcinoma · 2026Review
- Cutaneous Lupus Features Specialized Stromal Niches and Altered Retroelement Expression.The Journal of investigative dermatology · 2025Article
- LINE-1 retrotransposition in a mouse TDP-43 model of neurodegeneration marks motor cortex neurons for cell-intrinsic and cell non-autonomous programmed cell death.PLoS genetics · 2025Article
- H3K27 and H3K9 methylation mask potential CTCF binding sites to maintain 3D genome integrity.Genome research · 2025Article
- Combination Therapy Approaches to Enhance the Efficacy of ERV-Targeting Vaccines in Cancer.Cancer immunology research · 2025Review
- The SUV39 Family of H3K9 Methyltransferases in Skeletal Muscle Stem Cells.FASEB bioAdvances · 2025Review
- Identification and clinical implications of endogenous retrovirus elements suppressed by SETDB1 in hepatocellular carcinoma.JHEP reports : innovation in hepatology · 2025Article
- Stem cell activity-coupled suppression of endogenous retrovirus governs adult tissue regeneration.Cell · 2024Article
- Article
- SETDB1 activity is globally directed by H3K14 acetylation via its Triple Tudor Domain.Nucleic acids research · 2024Article
- SETDB1 regulates short interspersed nuclear elements and chromatin loop organization in mouse neural precursor cells.Genome biology · 2024Article
- SETDB1 as a cancer target: challenges and perspectives in drug design.RSC medicinal chemistry · 2024Review
- Activation of endogenous retroviruses and induction of viral mimicry by MEK1/2 inhibition in pancreatic cancer.Science advances · 2024Article
- Cell-type differential targeting of SETDB1 prevents aberrant CTCF binding, chromatin looping, and cis-regulatory interactions.Nature communications · 2024Article
10 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Subsets of endogenous retroviruses (ERVs) are derepressed in mouse embryonic stem cells (mESCs) deficient for Setdb1, which catalyzes histone H3 lysine 9 trimethylation (H3K9me3). Most of those ERVs, including IAPs, remain silent if Setdb1 is deleted in differentiated embryonic cells; however they are derepressed when deficient for Dnmt1, suggesting that Setdb1 is dispensable for ERV silencing in somatic cells. However, H3K9me3 enrichment on ERVs is maintained in differentiated cells and is mostly diminished in mouse embryonic fibroblasts (MEFs) lacking Setdb1. Here we find that distinctive sets of ERVs are reactivated in different types of Setdb1-deficient somatic cells, including the VL30-class of ERVs in MEFs, whose derepression is dependent on cell-type-specific transcription factors (TFs). These data suggest a more general role for Setdb1 in ERV silencing, which provides an additional layer of epigenetic silencing through the H3K9me3 modification.
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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.