ArticleGenes & development2013
Lamin B1 depletion in senescent cells triggers large-scale changes in gene expression and the chromatin landscape.
Article in Genes & development, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 337 papers.
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Who cites it
337 citing papers in PubMed, 549 citations in OpenAlex.
- Age-Related Lamin B1 Deficiency Activates SLC7A11-Dependent Disulfidptosis to Impair Osteogenesis via Intercepting Mitochondrial Fission.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Protracted Fate Acquisition and Epigenetic De-Aging During Induced Neural Stem Cell Conversion of Human Blood Cells.Aging cell · 2026Article
- Senescent cells cluster CTCF on nuclear speckles to instruct an alternative splicing program.Nature aging · 2026Article
- Quercetin Mitigates Oxidative Stress-Induced Premature Senescence in SH-SY5Y Neuronal-like Cells.International journal of molecular sciences · 2026Article
- Molecular mechanisms and recent advances in cellular senescence.Cell & bioscience · 2026Review
- Transcription-independent induction of rapid-onset senescence is integral to healing.Nature cell biology · 2026Article
- Lamin B1 safeguards the B cell genome and shapes lymphoma outcome.HemaSphere · 2026Article
- Review
- Dysregulated nuclear Lamin B1 in DYT1 dystonia thickens nuclear lamina and disrupts 14-3-3 proteins.Cell death discovery · 2026Article
- Tiki2 restrains Wnt5a/Ror signaling to limit inflammation in acute kidney injury.Communications biology · 2026Article
- The Emerging Role of Senolytics as a Next-Generation Strategy Against Glioma Recurrence: A Narrative Review.Cancers · 2026Review
- Review
- Senescence profiling and biomarker identification in cell product based on adipose tissue-derived mesenchymal stromal cells.Stem cells translational medicine · 2026Article
- "Metabolic memory" of aging: anchoring, transmission, and frontiers of transgenerational intervention.Biogerontology · 2026Review
- BAP1 Loss Induces Senescence and Enhances the Response to Radiation Therapy and Senolytics.bioRxiv : the preprint server for biology · 2026Article
- Introducing Cellular Senescence in Human Induced Pluripotent Stem Cells and Differentiated Neural Lineage for Modeling of Age-Associated Diseases.Advanced biology · 2026Article
- Autophagy as an adaptive resistance mechanism to epigenetic therapy in cancer.Frontiers in oncology · 2026Review
- From molecular damage to regulatory constraint: epigenetic and metabolic limits of cellular plasticity in aging.Frontiers in aging · 2026Review
- The intricate interplay between circadian rhythm, androgen signaling, hormone therapy, and cellular senescence in prostate cancer.Cancer metastasis reviews · 2025Review
- Unravelling the genetics and epigenetics of the ageing tumour microenvironment in cancer.Nature reviews. Cancer · 2025Review
277 more citing papers are in PubMed but not listed here.
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Authors and funding
13 authors at 2 institutions in 2 countries.
Funding
Abstract
Senescence is a stable proliferation arrest, associated with an altered secretory pathway, thought to promote tumor suppression and tissue aging. While chromatin regulation and lamin B1 down-regulation have been implicated as senescence effectors, functional interactions between them are poorly understood. We compared genome-wide Lys4 trimethylation on histone H3 (H3K4me3) and H3K27me3 distributions between proliferating and senescent human cells and found dramatic differences in senescence, including large-scale domains of H3K4me3- and H3K27me3-enriched "mesas" and H3K27me3-depleted "canyons." Mesas form at lamin B1-associated domains (LADs) in replicative senescence and oncogene-induced senescence and overlap DNA hypomethylation regions in cancer, suggesting that pre-malignant senescent chromatin changes foreshadow epigenetic cancer changes. Hutchinson-Gilford progeria syndrome fibroblasts (mutant lamin A) also show evidence of H3K4me3 mesas, suggesting a link between premature chromatin changes and accelerated cell senescence. Canyons mostly form between LADs and are enriched in genes and enhancers. H3K27me3 loss is correlated with up-regulation of key senescence genes, indicating a link between global chromatin changes and local gene expression regulation. Lamin B1 reduction in proliferating cells triggers senescence and formation of mesas and canyons. Our data illustrate profound chromatin reorganization during senescence and suggest that lamin B1 down-regulation in senescence is a key trigger of global and local chromatin changes that impact gene expression, aging, and cancer.
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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.