ArticleMolecular and cellular biology2017
Progerin-Induced Replication Stress Facilitates Premature Senescence in Hutchinson-Gilford Progeria Syndrome.
Article in Molecular and cellular biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 67 citations in OpenAlex.
- Inhibiting Glutaminase Reverses Senescence-Associated Mitochondrial Dysfunction and Skeletal Muscle Decline.Aging cell · 2026Article
- The senescence-inhibitory p53 isoform Δ133p53α: enhancing cancer immunotherapy and exploring novel therapeutic approaches for senescence-associated diseases.GeroScience · 2026Review
- Expression of progerin enhances disease-related endpoints in a tau seeding reporter cell system.GeroScience · 2026Article
- BMI1 represses G-quadruplex DNA formation to maintain genomic stability during replication.The Journal of biological chemistry · 2026Article
- Recurrent somatic mutation and progerin expression in early vascular aging of chronic kidney disease.Nature aging · 2025Article
- Pharmacologic activation of Δ133p53α reduces cellular senescence in progeria patients-derived cells.Aging pathobiology and therapeutics · 2025Article
- VPS4B orchestrates response to nuclear envelope stress by regulating ESCRT-III dynamics in glioblastoma.Nucleus (Austin, Tex.) · 2024Article
- A defective splicing machinery promotes senescence through MDM4 alternative splicing.Aging cell · 2024Article
- Umbilical cord mesenchymal stem cells in ulcerative colitis treatment: efficacy and possible mechanisms.Stem cell research & therapy · 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
- Progerin Can Induce DNA Damage in the Absence of Global Changes in Replication or Cell Proliferation.bioRxiv : the preprint server for biology · 2024Article
- Progeria-based vascular model identifies networks associated with cardiovascular aging and disease.Aging cell · 2024Article
- Replication stress as a driver of cellular senescence and aging.Communications biology · 2024Review
- Genetic and pharmacological modulation of lamin A farnesylation determines its function and turnover.Aging cell · 2024Article
- Progerin can induce DNA damage in the absence of global changes in replication or cell proliferation.PloS one · 2024Article
- Limitations of human brain organoids to study neurodegenerative diseases: a manual to survive.Frontiers in cellular neuroscience · 2024Review
- Mechanotransduction of the vasculature in Hutchinson-Gilford Progeria Syndrome.Frontiers in physiology · 2024Review
- The organizer of chromatin topology RIF1 ensures cellular resilience to DNA replication stress.Life science alliance · 2023Article
- The Molecular and Cellular Basis of Hutchinson-Gilford Progeria Syndrome and Potential Treatments.Genes · 2023Review
- Senotherapeutics: An emerging approach to the treatment of viral infectious diseases in the elderly.Frontiers in cellular and infection microbiology · 2023Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Hutchinson-Gilford progeria syndrome (HGPS) is caused by a mutation in LMNA that produces an aberrant lamin A protein, progerin. The accumulation of progerin in HGPS cells leads to an aberrant nuclear morphology, genetic instability, and p53-dependent premature senescence. How p53 is activated in response to progerin production is unknown. Here we show that young cycling HGPS fibroblasts exhibit chronic DNA damage, primarily in S phase, as well as delayed replication fork progression. We demonstrate that progerin binds to PCNA, altering its distribution away from replicating DNA in HGPS cells, leading to γH2AX formation, ATR activation, and RPA Ser33 phosphorylation. Unlike normal human cells that can be immortalized by enforced expression of telomerase alone, immortalization of HGPS cells requires telomerase expression and p53 repression. In addition, we show that the DNA damage response in HGPS cells does not originate from eroded telomeres. Together, these results establish that progerin interferes with the coordination of essential DNA replication factors, causing replication stress, and is the primary signal for p53 activation leading to premature senescence in HGPS. Furthermore, this damage response is shown to be independent of progerin farnesylation, implying that unprocessed lamin A alone causes replication stress.
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Registered trials
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