ReviewNucleus (Austin, Tex.)2018
Genomic instability and DNA replication defects in progeroid syndromes.
Review in Nucleus (Austin, Tex.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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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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
32 citing papers in PubMed, 58 citations in OpenAlex.
- Telomeres in mitosis: organization and dynamics.Nucleus (Austin, Tex.) · 2026Review
- Network-driven discovery of repurposable drugs targeting hallmarks of aging.Nature aging · 2026Article
- The aging genome exhibits organized vulnerability to somatic mutations.bioRxiv : the preprint server for biology · 2026Article
- A manually curated gene-phenotype catalogue for progeroid syndromes and premature aging.Aging · 2026Article
- Article
- Article
- Progerin Can Induce DNA Damage in the Absence of Global Changes in Replication or Cell Proliferation.bioRxiv : the preprint server for biology · 2024Article
- Review
- Senescence, regulators of alternative splicing and effects of trametinib treatment in progeroid syndromes.GeroScience · 2024Article
- Progerin can induce DNA damage in the absence of global changes in replication or cell proliferation.PloS one · 2024Article
- Genomic Instability and Epigenetic Changes during Aging.International journal of molecular sciences · 2023Review
- ATXN3 controls DNA replication and transcription by regulating chromatin structure.Nucleic acids research · 2023Article
- Article
- Filamentous nuclear actin regulation of PML NBs during the DNA damage response is deregulated by prelamin A.Cell death & disease · 2022Article
- Genetic Ablation of the DNA Damage Response Pathway Attenuates Lamin-Associated Dilated Cardiomyopathy in Mice.JACC. Basic to translational science · 2022Article
- VRK1 Is a Synthetic-Lethal Target in VRK2-Deficient Glioblastoma.Cancer research · 2022Article
- Combined alteration of lamin and nuclear morphology influences the localization of the tumor-associated factor AKTIP.Journal of experimental & clinical cancer research : CR · 2022Article
- Article
- Genetic basis of cardiovascular aging is at the core of human longevity.The journal of cardiovascular aging · 2022Article
- Aging of the Retina: Molecular and Metabolic Turbulences and Potential Interventions.Annual review of vision science · 2021Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Progeroid syndromes induced by mutations in lamin A or in its interactors - named progeroid laminopathies - are model systems for the dissection of the molecular pathways causing physiological and premature aging. A large amount of data, based mainly on the Hutchinson Gilford Progeria syndrome (HGPS), one of the best characterized progeroid laminopathy, has highlighted the role of lamins in multiple DNA activities, including replication, repair, chromatin organization and telomere function. On the other hand, the phenotypes generated by mutations affecting genes directly acting on DNA function, as mutations in the helicases WRN and BLM or in the polymerase polδ, share many of the traits of progeroid laminopathies. These evidences support the hypothesis of a concerted implication of DNA function and lamins in aging. We focus here on these aspects to contribute to the comprehension of the driving forces acting in progeroid syndromes and premature aging.
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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.