ArticleMolecular cell2012
Independence of repressive histone marks and chromatin compaction during senescent heterochromatic layer formation.
Article in Molecular cell, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 207 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
207 citing papers in PubMed, 309 citations in OpenAlex.
- LINE-1 Deregulation in Ovarian Cancer: Implications for Diagnosis, Prognosis, and Therapeutic Targeting.Molecular diagnosis & therapy · 2026Review
- Senescent cells cluster CTCF on nuclear speckles to instruct an alternative splicing program.Nature aging · 2026Article
- Host-Pathogen Interaction as a Driver of Cellular Senescence: Microbial Triggers and Host Response.International journal of molecular sciences · 2026Review
- Histone mark remodeling in cancer: an enhancer-centered perspective.Genes & genomics · 2026Review
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- RPA hyperphosphorylation hinders the resolution of R-loops and G-quadruplex-associated R-loops during RAS-driven senescence.Nucleic acids research · 2026Article
- Review
- AI-assisted protein design to rapidly convert antibody sequences to intrabodies targeting diverse peptides and histone modifications.Science advances · 2026Article
- Spatial Reorganization of Chromatin Architecture Shapes the Expression Phenotype of Therapy-Induced Senescent Cells.Aging cell · 2026Article
- Biomarkers of ageing of humans and non-human primates.Nature reviews. Molecular cell biology · 2025Review
- Advancing biological understanding of cellular senescence with computational multiomics.Nature genetics · 2025Review
- Interrogating the regulatory epigenome of cellular senescence.Cellular and molecular life sciences : CMLS · 2025Review
- Perturb-tracing enables high-content screening of multi-scale 3D genome regulators.Nature methods · 2025Article
- AI-assisted protein design to rapidly convert antibody sequences to intrabodies targeting diverse peptides and histone modifications.bioRxiv : the preprint server for biology · 2025Article
- Studying Cellular Senescence Using the Model Organism Drosophila melanogaster.Methods in molecular biology (Clifton, N.J.) · 2025Article
- UTX/Top2β axis mediated spinal cord microvascular endothelial cells senescence exacerbates spinal cord injury.PloS one · 2025Article
- Epigenetic regulation of reprogramming and pluripotency: insights from histone modifications and their implications for cancer stem cell therapies.Frontiers in cell and developmental biology · 2025Review
- Dynamic 3D genome reorganization during senescence: defining cell states through chromatin.Cell death and differentiation · 2025Article
- Article
- Interplay between epigenetics, senescence and cellular redox metabolism in cancer and its therapeutic implications.Redox biology · 2024Review
147 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
29 authors at 12 institutions in 5 countries.
Funding
Abstract
The expansion of repressive epigenetic marks has been implicated in heterochromatin formation during embryonic development, but the general applicability of this mechanism is unclear. Here we show that nuclear rearrangement of repressive histone marks H3K9me3 and H3K27me3 into nonoverlapping structural layers characterizes senescence-associated heterochromatic foci (SAHF) formation in human fibroblasts. However, the global landscape of these repressive marks remains unchanged upon SAHF formation, suggesting that in somatic cells, heterochromatin can be formed through the spatial repositioning of pre-existing repressively marked histones. This model is reinforced by the correlation of presenescent replication timing with both the subsequent layered structure of SAHFs and the global landscape of the repressive marks, allowing us to integrate microscopic and genomic information. Furthermore, modulation of SAHF structure does not affect the occupancy of these repressive marks, nor vice versa. These experiments reveal that high-order heterochromatin formation and epigenetic remodeling of the genome can be discrete events.
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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.