ArticleAging cell2020
PML2-mediated thread-like nuclear bodies mark late senescence in Hutchinson-Gilford progeria syndrome.
Article in Aging cell, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 18 citations in OpenAlex.
- Repair and misrepair of telomeric DNA in dynamic interactions with PML nuclear bodies and lamin B1 in doxorubicin-treated cancer cells.Nucleus (Austin, Tex.) · 2026Article
- Patching up the nucleus: a novel role for PMLII in nuclear envelope stability.Nucleic acids research · 2026Article
- Biomarkers of ageing of humans and non-human primates.Nature reviews. Molecular cell biology · 2025Review
- Design principles of gene circuits for longevity.Trends in cell biology · 2025Review
- The syntaxin-binding protein STXBP5 regulates progerin expression.Scientific reports · 2024Article
- Article
- Doxycycline decelerates aging in progeria mice.Aging cell · 2024Article
- PML modulates epigenetic composition of chromatin to regulate expression of pro-metastatic genes in triple-negative breast cancer.Nucleic acids research · 2023Article
- Biomarkers of aging.Science China. Life sciences · 2023Review
- Filamentous nuclear actin regulation of PML NBs during the DNA damage response is deregulated by prelamin A.Cell death & disease · 2022Article
- A Glb1-2A-mCherry reporter monitors systemic aging and predicts lifespan in middle-aged mice.Nature communications · 2022Article
- Progerin modulates the IGF-1R/Akt signaling involved in aging.Science advances · 2022Article
- Running 'LAPS' Around nLD: Nuclear Lipid Droplet Form and Function.Frontiers in cell and developmental biology · 2022Review
- PML2-mediated thread-like nuclear bodies mark late senescence in Hutchinson-Gilford progeria syndrome.Aging cell · 2020Article
Corrections and comments
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Authors and funding
15 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Progerin accumulation disrupts nuclear lamina integrity and causes nuclear structure abnormalities, leading to premature aging, that is, Hutchinson-Gilford progeria syndrome (HGPS). The roles of nuclear subcompartments, such as PML nuclear bodies (PML NBs), in HGPS pathogenesis, are unclear. Here, we show that classical dot-like PML NBs are reorganized into thread-like structures in HGPS patient fibroblasts and their presence is associated with late stage of senescence. By co-immunoprecipitation analysis, we show that farnesylated Progerin interacts with human PML2, which accounts for the formation of thread-like PML NBs. Specifically, human PML2 but not PML1 overexpression in HGPS cells promotes PML thread development and accelerates senescence. Further immunofluorescence microscopy, immuno-TRAP, and deep sequencing data suggest that these irregular PML NBs might promote senescence by perturbing NB-associated DNA repair and gene expression in HGPS cells. These data identify irregular structures of PML NBs in senescent HGPS cells and support that the thread-like PML NBs might be a novel, morphological, and functional biomarker of late senescence.
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