ArticleNature communications2017
Nucleolar expansion and elevated protein translation in premature aging.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 174 papers.
What it found
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Who cites it
174 citing papers in PubMed, 266 citations in OpenAlex.
- Article
- Muscular dystrophy-associated lamin variants disrupt cellular organization through a nucleolar-ribosomal axis.Science advances · 2026Article
- Beyond the Ribosome: The Expanding Role of the Nucleolus in Neurodegenerative Pathways.Molecular neurobiology · 2026Review
- The Nucleolus in Human Disease: Ribosome Biogenesis, Nucleolar Surveillance, and Therapeutic Opportunities.Biomolecules · 2026Review
- Nuclear envelope-dependent heterochromatin positioning gates the timing of nucleolar assembly in the early embryo.bioRxiv : the preprint server for biology · 2026Article
- Deciphering the impact ofGenes & diseases · 2026Article
- Age-related decline in niche self-renewal factors drives testis aging via Hairless, Imp, and Chinmo.Science advances · 2026Article
- Nuclear Lamina Dysfunction and DNA Damage as Drivers of Premature Senescence in a Human Müller Glial Cell Model of Spinocerebellar Ataxia Type 7.International journal of molecular sciences · 2026Article
- Embryo-scale Visual Cell Sorting reveals a conserved transcriptomic signature of nucleolar size linked to proteostasis.bioRxiv : the preprint server for biology · 2026Article
- Telomere Dysfunction in Human Astrocytes Drives Acrocentric Chromosome Instability and Nucleolar Reorganization.bioRxiv : the preprint server for biology · 2026Article
- Cardiomyocyte-Specific Plakophilin-2 Loss Is Sufficient to Induce Aging and Senescence of Nonmyocytes: Relevance to Arrhythmogenic Cardiomyopathy.Journal of the American Heart Association · 2026Article
- Exceptional Longevity Modifying Allele APOE2 Promotes DNA Signaling Pathways Resisting Cellular Senescence in Human Neurons.Aging cell · 2026Article
- RUNX1-deficiency drives immune-active ERbioRxiv : the preprint server for biology · 2026Article
- Lifelong behavioral screen reveals an architecture of vertebrate aging.Science (New York, N.Y.) · 2026Article
- Recent Advances in Proximity Labeling-Based Subcellular Proteomic Mapping.Molecular & cellular proteomics : MCP · 2026Review
- Supercoils Stabilize a "DNA Corset" Condensate with Torsion-Dependent Hysteretic Compaction.JACS Au · 2026Article
- Article
- Mechanobiology of the Nucleolus.Biology of the cell · 2026Review
- Nucleolar expansion: A biomolecular condensate mortality timer.Geromedicine · 2026Article
- SIRT1/DNMT3B-mediated epigenetic gene silencing in response to phytoestrogens in mammary epithelial cells.Epigenetics · 2025Article
114 more citing papers are in PubMed but not listed here.
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Premature aging disorders provide an opportunity to study the mechanisms that drive aging. In Hutchinson-Gilford progeria syndrome (HGPS), a mutant form of the nuclear scaffold protein lamin A distorts nuclei and sequesters nuclear proteins. We sought to investigate protein homeostasis in this disease. Here, we report a widespread increase in protein turnover in HGPS-derived cells compared to normal cells. We determine that global protein synthesis is elevated as a consequence of activated nucleoli and enhanced ribosome biogenesis in HGPS-derived fibroblasts. Depleting normal lamin A or inducing mutant lamin A expression are each sufficient to drive nucleolar expansion. We further show that nucleolar size correlates with donor age in primary fibroblasts derived from healthy individuals and that ribosomal RNA production increases with age, indicating that nucleolar size and activity can serve as aging biomarkers. While limiting ribosome biogenesis extends lifespan in several systems, we show that increased ribosome biogenesis and activity are a hallmark of premature aging.HGPS is a premature aging disease caused by mutations in the nuclear protein lamin A. Here, the authors show that cells from patients with HGPS have expanded nucleoli and increased protein synthesis, and report that nucleoli also expand as aging progresses in cells derived from healthy individuals.
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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.