ArticleGenome research2018
Switching roles for DNA and histone methylation depend on evolutionary ages of human endogenous retroviruses.
Article in Genome research, 2018. 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, 129 citations in OpenAlex.
- Transposable elements in hematopoietic stem cells upon aging and myeloid malignancies.Mobile DNA · 2026Review
- Retroviral Remnants in the Human Genome: Classification, Integration and Regulation.Molecular diagnosis & therapy · 2026Review
- Endogenous retroviruses and response to immune checkpoint inhibitors: mechanisms, clinical evidence, and therapeutic implications.Frontiers in immunology · 2026Review
- Overcoming immunotherapy barriers in pediatric brain tumors: epigenetic strategies.Frontiers in oncology · 2026Review
- Endogenous retroviruses in aging and cancer: from genomic defense to oncogenic activation.Mobile DNA · 2025Review
- The expression, regulation, and function of human endogenous retroviruses in genitourinary cancers.Cell death discovery · 2025Review
- Ribosome dysregulation and intervention in age-related infertility.Cell reports. Medicine · 2025Article
- Optimized derivation and culture system of human naïve pluripotent stem cells with enhanced DNA methylation status and genomic stability.Protein & cell · 2025Article
- Roles of transposable elements and DNA methylation in the formation of CpG islands and CpG-depleted regulatory elements.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Epigenetic motifs distinguishing endogenous from exogenous retroviral integrants.Journal of virology · 2025Article
- The Role of Human Endogenous Retroviruses in the Initiation and Progression of Melanoma.Biomedicines · 2025Review
- Co-targeting of epigenetic regulators and BCL-XL improves efficacy of immune checkpoint blockade therapy in multiple solid tumors.Molecular cancer · 2025Article
- Binding of NF-Y to transposable elements in mouse and human cells.Mobile DNA · 2025Article
- DNA methylation in melanoma immunotherapy: mechanisms and therapeutic opportunities.Clinical epigenetics · 2025Review
- Unleashing viral mimicry: A combinatorial strategy to enhance the efficacy of PARP7 inhibitors.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025Review
- Mutation Rate Variation and Other Challenges in 2-LTR Dating of Primate Endogenous Retrovirus Integrations.Journal of molecular evolution · 2025Review
- On correlative and causal links of replicative epimutations.Trends in genetics : TIG · 2025Review
- H3K9me3 loss and ERVs activation as hallmarks for osteoarthritis progression and knee joint aging.Osteoarthritis and cartilage · 2025Article
- Endogenous retroelements in hematological malignancies: From epigenetic dysregulation to therapeutic targeting.American journal of hematology · 2025Review
- Activation of Evolutionarily Young Endogenous Retroviruses Is Implicated in COVID-19 Immunopathology.Genes to cells : devoted to molecular & cellular mechanisms · 2025Article
15 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
We provide a comprehensive genomic and epigenomic map of the more than 500,000 endogenous retroviruses (ERVs) and fragments that populate the intergenic regions of the human genome. The repressive epigenetic marks associated with the ERVs, particularly long terminal repeats (LTRs), show a remarkable switch in silencing mechanisms, depending on the evolutionary age of the LTRs. Young LTRs tend to be CpG rich and are mainly suppressed by DNA methylation, whereas intermediate age LTRs are associated predominantly with histone modifications, particularly histone H3 lysine 9 (H3K9) methylation. Young LTRs can be reactivated by treatment with the DNA methylation inhibitor 5-aza-2'-deoxycytidine (5-aza-CdR) alone, but their level of expression is much increased by 5-aza-CdR treatment plus knockdown of one of several H3K9 methyltransferases or of the H3K27 methyltransferase EZH2. The removal of cytosine methylation led to rapid, widespread increases in H3K9me3 in the LTRs. Intermediate age LTRs had lower CpG densities and were not up-regulated by 5-aza-CdR treatment, but they were sensitive to knockdown of H3K9 methyltransferases. Unlike the situation in embryonic stem cells, the polycomb repressive complex (PRC2) has a minor role in LTR suppression by itself and is only a player after removal of cytosine methylation in the analyzed cancer cell line. Up-regulation of LTRs and induction of "viral mimicry" is rapidly becoming of interest for predicting cancer patient response to epigenetic therapies. Understanding the mechanism for LTR suppression is of major importance in order to improve patient treatment strategies.
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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 Socratic graph.