ArticleMolecular and cellular biology2014
The tumor suppressor PML specifically accumulates at RPA/Rad51-containing DNA damage repair foci but is nonessential for DNA damage-induced fibroblast senescence.
Article in Molecular and cellular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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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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Who cites it
11 citing papers in PubMed, 33 citations in OpenAlex.
- Article
- Early onset senescence and cognitive impairment in a murine model of repeated mTBI.Acta neuropathologica communications · 2021Article
- Targeting Cell Senescence for the Treatment of Age-Related Bone Loss.Current osteoporosis reports · 2019Review
- Pml nuclear body disruption cooperates in APL pathogenesis and impairs DNA damage repair pathways in mice.Blood · 2018Article
- Multimodal Light Microscopy Approaches to Reveal Structural and Functional Properties of Promyelocytic Leukemia Nuclear Bodies.Frontiers in oncology · 2018Review
- PML nuclear body disruption impairs DNA double-strand break sensing and repair in APL.Cell death & disease · 2016Article
- Conserved Senescence Associated Genes and Pathways in Primary Human Fibroblasts Detected by RNA-Seq.PloS one · 2016Article
- Nesprin-2-dependent ERK1/2 compartmentalisation regulates the DNA damage response in vascular smooth muscle cell ageing.Cell death and differentiation · 2015Article
- Hormetic effect of rotenone in primary human fibroblasts.Immunity & ageing : I & A · 2015Article
- Effects of ebselen and N-acetyl cysteine on replicative aging of primary human fibroblast strains.Immunity & ageing : I & A · 2015Article
- Spots, damn'd spots and γH2AX foci.Cell cycle (Georgetown, Tex.) · 2015Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The PML tumor suppressor has been functionally implicated in DNA damage response and cellular senescence. Direct evidence for such a role based on PML knockdown or knockout approaches is still lacking. We have therefore analyzed the irradiation-induced DNA damage response and cellular senescence in human and mouse fibroblasts lacking PML. Our data show that PML nuclear bodies (NBs) nonrandomly associate with persistent DNA damage foci in unperturbed human skin and in high-dose-irradiated cell culture systems. PML bodies do not associate with transient γH2AX foci after low-dose gamma irradiation. Superresolution microscopy reveals that all PML bodies within a nucleus are engaged at Rad51- and RPA-containing repair foci during ongoing DNA repair. The lack of PML (i) does not majorly affect the DNA damage response, (ii) does not alter the efficiency of senescence induction after DNA damage, and (iii) does not affect the proliferative potential of primary mouse embryonic fibroblasts during serial passaging. Thus, while PML NBs specifically accumulate at Rad51/RPA-containing lesions and senescence-derived persistent DNA damage foci, they are not essential for DNA damage-induced and replicative senescence of human and murine fibroblasts.
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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.