ReviewCurrent opinion in cell biology2015
DNA repair defects and genome instability in Hutchinson-Gilford Progeria Syndrome.
Review in Current opinion in cell biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
83 citing papers in PubMed, 134 citations in OpenAlex.
- Mutation-agnostic base editing of the progerin farnesylation site rescues Hutchinson-Gilford progeria syndrome phenotypes in neuromuscular organoids.Nature communications · 2026Article
- Cellular senescence and aging: molecular mechanisms and convergent pathways.Cellular and molecular life sciences : CMLS · 2026Review
- Nuclear dysfunction in aging and neurodegeneration.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Review
- Essential Role for Telomeric Repeat-Binding Factor 2 in Cardiac Development and Function.FASEB bioAdvances · 2026Article
- Increased Telomere Mobility in Progeria is Restored by Isoprenylcysteine Carboxyl Methyltransferase Inhibition.bioRxiv : the preprint server for biology · 2026Article
- A study on the nutritional status and body composition of children with Hutchinson-Gilford progeria syndrome.Orphanet journal of rare diseases · 2026Article
- Nuclear envelope proteins in cancer: revisiting the significance of LEM-domain proteins.Frontiers in cell and developmental biology · 2026Review
- The Converging Roles of Nucleases and Helicases in Genome Maintenance and the Aging Process.Life (Basel, Switzerland) · 2025Review
- The dual guardians of cellular stability: exploring nesprin and lamin in senescence.Cell death & disease · 2025Review
- Targeting DNA damage in ageing: towards supercharging DNA repair.Nature reviews. Drug discovery · 2025Review
- Patient-Derived Cortical Organoids Reveal Senescence of Neural Progenitor Cells in Hutchinson-Gilford Progeria Syndrome.Aging cell · 2025Article
- Article
- A multiparametric anti-aging CRISPR screen uncovers a role for BAF in protein synthesis regulation.Nature communications · 2025Article
- The intersection of TREX1, cGAS, STING and the DNA damage theory of aging.Frontiers in aging · 2025Review
- The Significance of the Response: Beyond the Mechanics of DNA Damage and Repair-Physiological, Genetic, and Systemic Aspects of Radiosensitivity in Higher Organisms.International journal of molecular sciences · 2024Review
- Normal Bone Matrix Mineralization but Altered Growth Plate Morphology in the LmnaAging and disease · 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
- Review
- Progerin Can Induce DNA Damage in the Absence of Global Changes in Replication or Cell Proliferation.bioRxiv : the preprint server for biology · 2024Article
- Progerin Inhibits the Proliferation and Migration of Melanoma Cells by Regulating the Expression of Paxillin.OncoTargets and therapy · 2024Article
23 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The integrity of the nuclear lamina has emerged as an important factor in the maintenance of genome stability. In particular, mutations in the LMNA gene, encoding A-type lamins (lamin A/C), alter nuclear morphology and function, and cause genomic instability. LMNA gene mutations are associated with a variety of degenerative diseases and devastating premature aging syndromes such as Hutchinson-Gilford Progeria Syndrome (HGPS) and Restrictive Dermopathy (RD). HGPS is a severe laminopathy, with patients dying in their teens from myocardial infarction or stroke. HGPS patient-derived cells exhibit nuclear shape abnormalities, changes in epigenetic regulation and gene expression, telomere shortening, genome instability, and premature senescence. This review highlights recent advances in identifying molecular mechanisms that contribute to the pathophysiology of HGPS, with a special emphasis on DNA repair defects and genome instability.
Indexed as
Identifiers
What OpenQuestion holds
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.