ArticleNucleus (Austin, Tex.)2016
Disruption of PCNA-lamins A/C interactions by prelamin A induces DNA replication fork stalling.
Article in Nucleus (Austin, Tex.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
28 citing papers in PubMed, 40 citations in OpenAlex.
- Nuclear dysfunction in aging and neurodegeneration.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Review
- Nuclear Lamins: A Molecular Bridge Coupling Extracellular Mechanical Cues to Intranuclear Signal Transduction and Gene Regulation.International journal of molecular sciences · 2026Review
- Mineral Stress Drives Loss of Heterochromatin: An Early Harbinger of Vascular Inflammaging and Calcification.Circulation research · 2025Article
- Phylloquinone improves endothelial function, inhibits cellular senescence, and vascular inflammation.GeroScience · 2024Article
- The Compromised Fanconi Anemia Pathway in Prelamin A-Expressing Cells Contributes to Replication Stress-Induced Genomic Instability.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Genetic and pharmacological modulation of lamin A farnesylation determines its function and turnover.Aging cell · 2024Article
- The organizer of chromatin topology RIF1 ensures cellular resilience to DNA replication stress.Life science alliance · 2023Article
- Lamin A to Z in normal aging.Aging · 2022Article
- Article
- TEX264 at the intersection of autophagy and DNA repair.Autophagy · 2022Review
- Review
- Diversity of Nuclear Lamin A/C Action as a Key to Tissue-Specific Regulation of Cellular Identity in Health and Disease.Frontiers in cell and developmental biology · 2021Review
- Towards delineating the chain of events that cause premature senescence in the accelerated aging syndrome Hutchinson-Gilford progeria (HGPS).Biochemical Society transactions · 2020Review
- Heterochromatin loss as a determinant of progerin-induced DNA damage in Hutchinson-Gilford Progeria.Aging cell · 2020Article
- The RXFP3 receptor is functionally associated with cellular responses to oxidative stress and DNA damage.Aging · 2019Article
- Lamin A/C Cardiomyopathy: Implications for Treatment.Current cardiology reports · 2019Review
- Genomic instability and innate immune responses to self-DNA in progeria.GeroScience · 2019Review
- Arterial "inflammaging" drives vascular calcification in children on dialysis.Kidney international · 2019Article
- Towards improving proximity labeling by the biotin ligase BirA.Methods (San Diego, Calif.) · 2019Article
- Genomic instability and DNA replication defects in progeroid syndromes.Nucleus (Austin, Tex.) · 2018Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The accumulation of prelamin A is linked to disruption of cellular homeostasis, tissue degeneration and aging. Its expression is implicated in compromised genome stability and increased levels of DNA damage, but to date there is no complete explanation for how prelamin A exerts its toxic effects. As the nuclear lamina is important for DNA replication we wanted to investigate the relationship between prelamin A expression and DNA replication fork stability. In this study we report that the expression of prelamin A in U2OS cells induced both mono-ubiquitination of proliferating cell nuclear antigen (PCNA) and subsequent induction of Pol η, two hallmarks of DNA replication fork stalling. Immunofluorescence microscopy revealed that cells expressing prelamin A presented with high levels of colocalisation between PCNA and γH2AX, indicating collapse of stalled DNA replication forks into DNA double-strand breaks. Subsequent protein-protein interaction assays showed prelamin A interacted with PCNA and that its presence mitigated interactions between PCNA and the mature nuclear lamina. Thus, we propose that the cytotoxicity of prelamin A arises in part, from it actively competing against mature lamin A to bind PCNA and that this destabilises DNA replication to induce fork stalling which in turn contributes to genomic instability.
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Registered trials
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.