ArticlePloS one2016
Loss of H3K9me3 Correlates with ATM Activation and Histone H2AX Phosphorylation Deficiencies in Hutchinson-Gilford Progeria Syndrome.
Article in PloS one, 2016. 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, 32 citations in OpenAlex.
- Article
- Expression of progerin enhances disease-related endpoints in a tau seeding reporter cell system.GeroScience · 2026Article
- Article
- Pharmacologic activation of Δ133p53α reduces cellular senescence in progeria patients-derived cells.Aging pathobiology and therapeutics · 2025Article
- SPIN1 facilitates chemoresistance and HR repair by promoting Tip60 binding to H3K9me3.EMBO reports · 2024Article
- Progeria-based vascular model identifies networks associated with cardiovascular aging and disease.Aging cell · 2024Article
- Senescence, regulators of alternative splicing and effects of trametinib treatment in progeroid syndromes.GeroScience · 2024Article
- The Role of β-Dystroglycan in Nuclear Dynamics.Cells · 2024Article
- Lamin A/C facilitates DNA damage response by modulating ATM signaling and homologous recombination pathways.Animal cells and systems · 2024Article
- Can accelerated ageing models inform us on age-related tauopathies?Aging cell · 2023Review
- Review
- MG132 Induces Progerin Clearance and Improves Disease Phenotypes in HGPS-like Patients' Cells.Cells · 2022Article
- Mechanisms of angiogenic incompetence in Hutchinson-Gilford progeria via downregulation of endothelial NOS.Aging cell · 2021Article
- Ultraviolet radiation protection potentials of Methylene Blue for human skin and coral reef health.Scientific reports · 2021Article
- Human WRN is an intrinsic inhibitor of progerin, abnormal splicing product of lamin A.Scientific reports · 2021Article
- Review
- SAMMY-seq reveals early alteration of heterochromatin and deregulation of bivalent genes in Hutchinson-Gilford Progeria Syndrome.Nature communications · 2020Article
- METTL3 counteracts premature aging via m6A-dependent stabilization of MIS12 mRNA.Nucleic acids research · 2020Article
- Loss of Dystroglycan Drives Cellular Senescence via Defective Mitosis-Mediated Genomic Instability.International journal of molecular sciences · 2020Article
- Widespread loss of the silencing epigenetic mark H3K9me3 in astrocytes and neurons along with hippocampal-dependent cognitive impairment in C9orf72 BAC transgenic mice.Clinical epigenetics · 2020Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Compelling evidence suggests that defective DNA damage response (DDR) plays a key role in the premature aging phenotypes in Hutchinson-Gilford progeria syndrome (HGPS). Studies document widespread alterations in histone modifications in HGPS cells, especially, the global loss of histone H3 trimethylated on lysine 9 (H3K9me3). In this study, we explore the potential connection(s) between H3K9me3 loss and the impaired DDR in HGPS. When cells are exposed to a DNA-damaging agent Doxorubicin (Dox), double strand breaks (DSBs) are generated that result in the phosphorylation of histone H2A variant H2AX (gammaH2AX) within an hour. We find that the intensities of gammaH2AX foci appear significantly weaker in the G0/G1 phase HGPS cells compared to control cells. This reduction is associated with a delay in the recruitment of essential DDR factors. We further demonstrate that ataxia-telangiectasia mutated (ATM) is responsible for the amplification of gammaH2AX signals at DSBs during G0/G1 phase, and its activation is inhibited in the HGPS cells that display significant loss of H3K9me3. Moreover, methylene (MB) blue treatment, which is known to save heterochromatin loss in HGPS, restores H3K9me3, stimulates ATM activity, increases gammaH2AX signals and rescues deficient DDR. In summary, this study demonstrates an early DDR defect of attenuated gammaH2AX signals in G0/G1 phase HGPS cells and provides a plausible connection between H3K9me3 loss and DDR deficiency.
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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.