ArticleNucleic acids research2017
Histone H1 depletion triggers an interferon response in cancer cells via activation of heterochromatic repeats.
Article in Nucleic acids research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 71 citations in OpenAlex.
- Article
- H1.3 depletion in AML cells prompts H1.2 redistribution, chromatin remodeling and cell cycle defects.Epigenetics & chromatin · 2026Article
- SFPQ directs histone H3.3 deposition to R-loops in DNA repeats to protect genome stability.Nature communications · 2026Article
- A Proteoform-Resolved Atlas of Human Cardiac Histones.Research square · 2026Article
- The insider's perspective: The intracellular complosome and immune cell dynamics in cancer.Clinical and translational medicine · 2026Review
- Linker histone regulates the myeloid versus lymphoid bifurcation of multipotent hematopoietic stem and progenitors.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Unintegrated HIV-1 DNA recruits cGAS via its histone-binding domain to escape innate immunity.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Reducing batch effects in single cell chromatin accessibility measurements by pooled transposition with MULTI-ATAC.bioRxiv : the preprint server for biology · 2025Article
- Anticancer Plant Secondary Metabolites Evicting Linker Histone H1.2 from Chromatin Activate Type I Interferon Signaling.International journal of molecular sciences · 2025Article
- Anticancer Plant Secondary Metabolites Induce Linker Histone Depletion from Chromatin.Frontiers in bioscience (Landmark edition) · 2024Article
- Article
- Genomic profiling of six human somatic histone H1 variants denotes that H1X accumulates at recently incorporated transposable elements.Nucleic acids research · 2024Article
- Transcription of endogenous retroviruses in senescent cells contributes to the accumulation of double-stranded RNAs that trigger an anti-viral response that reinforces senescence.Cell death & disease · 2024Article
- RNA-Seq Analysis of Trans-Differentiated ARPE-19 Cells Transduced by AAV9-AIPL1 Vectors.International journal of molecular sciences · 2023Article
- The odyssey of cGAS: From cytosol to nucleus.Cytokine & growth factor reviews · 2023Review
- MacroH2A1.1 as a crossroad between epigenetics, inflammation and metabolism of mesenchymal stromal cells in myelodysplastic syndromes.Cell death & disease · 2023Article
- Megakaryopoiesis impairment through acute innate immune signaling activation by azacitidine.The Journal of experimental medicine · 2022Article
- Review
- Histone H1 regulates non-coding RNA turnover on chromatin in a m6A-dependent manner.Cell reports · 2022Article
- FACT subunit SUPT16H associates with BRD4 and contributes to silencing of interferon signaling.Nucleic acids research · 2022Article
Corrections and comments
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Authors and funding
13 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Histone H1 has seven variants in human somatic cells and contributes to chromatin compaction and transcriptional regulation. Knock-down (KD) of each H1 variant in breast cancer cells results in altered gene expression and proliferation differently in a variant specific manner with H1.2 and H1.4 KDs being most deleterious. Here we show combined depletion of H1.2 and H1.4 has a strong deleterious effect resulting in a strong interferon (IFN) response, as evidenced by an up-regulation of many IFN-stimulated genes (ISGs) not seen in individual nor in other combinations of H1 variant KDs. Although H1 participates to repress ISG promoters, IFN activation upon H1.2 and H1.4 KD is mainly generated through the activation of the IFN response by cytosolic nucleic acid receptors and IFN synthesis, and without changes in histone modifications at induced ISG promoters. H1.2 and H1.4 co-KD also promotes the appearance of accessibility sites genome wide and, particularly, at satellites and other repeats. The IFN response may be triggered by the expression of noncoding RNA generated from heterochromatic repeats or endogenous retroviruses upon H1 KD. In conclusion, redundant H1-mediated silencing of heterochromatin is important to maintain cell homeostasis and to avoid an unspecific IFN response.
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Registered trials
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