ArticleNature genetics2017
DNMT and HDAC inhibitors induce cryptic transcription start sites encoded in long terminal repeats.
Article in Nature genetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 203 papers.
What it found
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Who cites it
203 citing papers in PubMed, 332 citations in OpenAlex.
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- Transposable Element Activation: A Hallmark of Cancer.Cancer discovery · 2026Review
- SUMOylation enhances DNMT1 function to repress mega-intergenic RNAs and viral mimicry.Nature genetics · 2026Article
- SUMOylation fine-tunes DNMT1 to silence viral mimicry transcripts.Nature genetics · 2026Article
- Mitochondrial-Epigenetic Crosstalk in Autism Spectrum Disorder: Linking Cellular Stress to Synaptic Dysfunction and Treatment Resistance.Molecular neurobiology · 2026Review
- TIPs: a deep learning-guided proteogenomic framework to expand the landscape of transposable element-derived antigens with immunopeptidomics.Genome biology · 2026Article
- ToxiTaRGET: a multi-omics database for toxicant-responsive molecular targets.Nature communications · 2026Article
- Embryonic stem cell factors DPPA2/4 amplify active H3K4me3-H2AK119ub chromatin domains in non-small cell lung cancer.Genes & development · 2026Article
- Unannotated noncoding transcripts as a source of intratumor heterogeneity in malignant cell states.Science China. Life sciences · 2026Article
- Transposable elements shape stemness in normal and leukemic hematopoiesis.Nature genetics · 2026Article
- B-type lamins maintain transcriptional homeostasis by spatially controlling chromatin-speckle proximity.Nucleic acids research · 2026Article
- Transcriptomic landscape of transposable elements revealsGenome research · 2026Article
- Architectural and evolutionary features of TE-derived TSSs shape tissue-specific promoter activity in the human genome.Nature communications · 2026Article
- Activation of endogenous retroviruses in tumor cells and their immunomodulatory mechanisms: from molecular basis to clinical translation.Frontiers in oncology · 2026Review
143 more citing papers are in PubMed but not listed here.
Corrections and comments
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- Erratum issued
Authors and funding
34 authors at 3 institutions in 2 countries.
Funding
Abstract
Several mechanisms of action have been proposed for DNA methyltransferase and histone deacetylase inhibitors (DNMTi and HDACi), primarily based on candidate-gene approaches. However, less is known about their genome-wide transcriptional and epigenomic consequences. By mapping global transcription start site (TSS) and chromatin dynamics, we observed the cryptic transcription of thousands of treatment-induced non-annotated TSSs (TINATs) following DNMTi and HDACi treatment. The resulting transcripts frequently splice into protein-coding exons and encode truncated or chimeric ORFs translated into products with predicted abnormal or immunogenic functions. TINAT transcription after DNMTi treatment coincided with DNA hypomethylation and gain of classical promoter histone marks, while HDACi specifically induced a subset of TINATs in association with H2AK9ac, H3K14ac, and H3K23ac. Despite this mechanistic difference, both inhibitors convergently induced transcription from identical sites, as we found TINATs to be encoded in solitary long terminal repeats of the ERV9/LTR12 family, which are epigenetically repressed in virtually all normal cells.
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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.