ArticleThe EMBO journal2009
Novel roles for A-type lamins in telomere biology and the DNA damage response pathway.
Article in The EMBO journal, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 155 papers.
What it found
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Who cites it
155 citing papers in PubMed, 248 citations in OpenAlex.
- A toxic STING-SAMHD1 axis drives replication stress in progeria and cancer cells.Nucleic acids research · 2026Article
- STING causes replication stress and nascent DNA degradation via SAMHD1.bioRxiv : the preprint server for biology · 2026Article
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- KIF2A-mediated microtubule-dependent nuclear envelope invagination drives nonhomologous end joining.Nucleic acids research · 2026Article
- Computational Characterization of Pathogenic LMNA Missense Variants: Structural Instability, Altered Binding, and Conformational Dynamics.Human mutation · 2026Article
- Vibration-Mediated Recovery of Irradiated Osteocytes and Their Regulatory Role in Breast Cancer Bone Metastasis.Advanced healthcare materials · 2026Article
- Sterile inflammation in laminopathies.European journal of cell biology · 2025Review
- Mitochondria-Localized Nestin Protects Mesenchymal Stem Cells from Senescence by Maintaining Cristae Structure and Function.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The dual guardians of cellular stability: exploring nesprin and lamin in senescence.Cell death & disease · 2025Review
- Nuclear compression-mediated DNA damage drives ATR-dependent Lamin expression and mouse ESC differentiation.Nucleic acids research · 2025Article
- Nuclear deformability increases PARPi sensitivity in BRCA1-deficient cells by increasing microtubule-dependent DNA break mobility.Nature communications · 2025Article
- Lamin A/C Deficiency Drives Genomic Instability and Poor Survival in Small-Cell Lung Cancer through Increased R-loop Accumulation.bioRxiv : the preprint server for biology · 2025Article
- High matrix stiffness promotes senescence of type II alveolar epithelial cells by lysosomal degradation of lamin A/C in pulmonary fibrosis.Respiratory research · 2025Article
- Roles for the 3D genome in the cell cycle, DNA replication, and double strand break repair.Frontiers in cell and developmental biology · 2025Review
- Role of Nuclear Lamins in the Regulation of the Genome: Focus on CardioLaminopathy.Sub-cellular biochemistry · 2025Review
- Review
- LAP2α orchestrates alternative lengthening of telomeres suppression through telomeric heterochromatin regulation with HDAC1: unveiling a potential therapeutic target.Cell death & disease · 2024Article
- Nuclear lamin A/C phosphorylation by loss of androgen receptor leads to cancer-associated fibroblast activation.Nature communications · 2024Article
- Proximal telomeric decompaction due to telomere shortening drives FOXC1-dependent myocardial senescence.Nucleic acids research · 2024Article
- Replication stress as a driver of cellular senescence and aging.Communications biology · 2024Review
95 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
14 authors at 7 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A-type lamins are intermediate filament proteins that provide a scaffold for protein complexes regulating nuclear structure and function. Mutations in the LMNA gene are linked to a variety of degenerative disorders termed laminopathies, whereas changes in the expression of lamins are associated with tumourigenesis. The molecular pathways affected by alterations of A-type lamins and how they contribute to disease are poorly understood. Here, we show that A-type lamins have a key role in the maintenance of telomere structure, length and function, and in the stabilization of 53BP1, a component of the DNA damage response (DDR) pathway. Loss of A-type lamins alters the nuclear distribution of telomeres and results in telomere shortening, defects in telomeric heterochromatin, and increased genomic instability. In addition, A-type lamins are necessary for the processing of dysfunctional telomeres by non-homologous end joining, putatively through stabilization of 53BP1. This study shows new functions for A-type lamins in the maintenance of genomic integrity, and suggests that alterations of telomere biology and defects in DDR contribute to the pathogenesis of lamin-related diseases.
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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.