ArticleNature communications2019
CSB promoter downregulation via histone H3 hypoacetylation is an early determinant of replicative senescence.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 44 citations in OpenAlex.
- Inhibiting cyclin D1-CDK6 suppresses senescence-associated inflammatory gene expression and age-related functional decline.Nature aging · 2026Article
- Aging alters genomic instability at endogenous mutation hotspots in mice.Scientific reports · 2025Article
- Targeting CyclinD1-CDK6 to Mitigate Senescence-Driven Inflammation and Age-Associated Functional Decline.bioRxiv : the preprint server for biology · 2025Article
- The context-dependent effect of cellular senescence: From embryogenesis and wound healing to aging.Ageing research reviews · 2025Review
- A subset of human dermal fibroblasts overexpressing Cockayne syndrome group B protein resist UVB radiation-mediated premature senescence.Aging cell · 2025Article
- Therapeutic targeting of senescent cells in the CNS.Nature reviews. Drug discovery · 2024Review
- Young small extracellular vesicles rejuvenate replicative senescence by remodeling Drp1 translocation-mediated mitochondrial dynamics.Journal of nanobiotechnology · 2024Article
- Article
- DNA-PKcs regulates myogenesis in an Akt-dependent manner independent of induced DNA damage.Cell death and differentiation · 2023Article
- The impact of cellular senescence and senescence‑associated secretory phenotype in cancer‑associated fibroblasts on the malignancy of pancreatic cancer.Oncology reports · 2023Article
- Premature aging in genetic diseases: what conclusions can be drawn for physiological aging.Frontiers in aging · 2023Review
- Understanding the Impact of Obesity on Ageing in the Radiance of DNA Metabolism.The journal of nutrition, health & aging · 2023Review
- Engrailed homeobox 1 transcriptional regulation of COL22A1 inhibits nasopharyngeal carcinoma cell senescence through the G1/S phase arrest.Journal of cellular and molecular medicine · 2022Article
- Effects of Oxygen Tension for Membrane Lipidome Remodeling of Cockayne Syndrome Cell Models.Cells · 2022Article
- Precise Diabetic Wound Therapy: PLS Nanospheres Eliminate Senescent Cells via DPP4 Targeting and PARP1 Activation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- Blockage of ERCC6 Alleviates Spinal Cord Injury Through Weakening Apoptosis, Inflammation, Senescence, and Oxidative Stress.Frontiers in molecular biosciences · 2022Article
- Article
- TAD-like single-cell domain structures exist on both active and inactive X chromosomes and persist under epigenetic perturbations.Genome biology · 2021Article
- Cockayne syndrome group A and ferrochelatase finely tune ribosomal gene transcription and its response to UV irradiation.Nucleic acids research · 2021Article
- DRP1 Inhibition Rescues Mitochondrial Integrity and Excessive Apoptosis in CS-A Disease Cell Models.International journal of molecular sciences · 2021Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cellular senescence has causative links with ageing and age-related diseases, however, it remains unclear if progeroid factors cause senescence in normal cells. Here, we show that depletion of CSB, a protein mutated in progeroid Cockayne syndrome (CS), is the earliest known trigger of p21-dependent replicative senescence. CSB depletion promotes overexpression of the HTRA3 protease resulting in mitochondrial impairments, which are causally linked to CS pathological phenotypes. The CSB promoter is downregulated by histone H3 hypoacetylation during DNA damage-response. Mechanistically, CSB binds to the p21 promoter thereby downregulating its transcription and blocking replicative senescence in a p53-independent manner. This activity of CSB is independent of its role in the repair of UV-induced DNA damage. HTRA3 accumulation and senescence are partially rescued upon reduction of oxidative/nitrosative stress. These findings establish a CSB/p21 axis that acts as a barrier to replicative senescence, and link a progeroid factor with the process of regular ageing in human.
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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.