ArticleCell cycle (Georgetown, Tex.)2011
A dual role for A-type lamins in DNA double-strand break repair.
Article in Cell cycle (Georgetown, Tex.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers, 1 of them a synthesis that pooled it.
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Who cites it
83 citing papers in PubMed, 1 synthesis or guideline pooled it, 139 citations in OpenAlex.
- Overlapping syndromes in laminopathies: a meta-analysis of the reported literature.Acta myologica : myopathies and cardiomyopathies : official journal of the Mediterranean Society of Myology · 2013Pooled it
- Review
- Lamin A/C as a Molecular Link Between Nuclear Organization, Chromatin Dynamics, and Tumor Progression.Cells · 2026Review
- LMNA-PRKDC axis enhances DNA repair and promotes chemoresistance in glioblastoma.Cell death & disease · 2025Article
- Lamin A/C loss promotes R-loop-mediated genomic instability and poor survival in small-cell lung cancer.Proceedings of the National Academy of Sciences of the United States of America · 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
- DNA double-stranded breaks, a hallmark of aging, defined at the nucleotide resolution, are increased and associated with transcription in the cardiac myocytes in LMNA-cardiomyopathy.Cardiovascular research · 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
- Review
- Interplay and Dynamics of Chromatin Architecture and DNA Damage Response: An Overview.Cancers · 2025Review
- Radiation symptoms resemble laminopathies and the physical underlying cause may sit at the lamin A C-terminus.Molecular medicine (Cambridge, Mass.) · 2025Article
- Tubular Lamin- and Emerin-Lined Nuclear Envelope Invaginations Isolate Chromatin Domains for Gene Expression Regulation.Sub-cellular biochemistry · 2025Review
- LAP2α orchestrates alternative lengthening of telomeres suppression through telomeric heterochromatin regulation with HDAC1: unveiling a potential therapeutic target.Cell death & disease · 2024Article
- The N-terminal coiled-coil domain of Arabidopsis CROWDED NUCLEI 1 is required for nuclear morphology maintenance.Planta · 2024Article
- Lamin A/C facilitates DNA damage response by modulating ATM signaling and homologous recombination pathways.Animal cells and systems · 2024Article
- Impaired end joining induces cardiac atrophy in a Hutchinson-Gilford progeria mouse model.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Arabidopsis lamin-like proteins CRWN1 and CRWN2 interact with SUPPRESSOR OF NPR1-1 INDUCIBLE 1 and RAD51D to prevent DNA damage.The Plant cell · 2023Article
- AKT2-mediated nuclear deformation leads to genome instability during epithelial-mesenchymal transition.iScience · 2023Article
- Article
23 more citing papers are in PubMed but not listed here.
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Authors and funding
13 authors at 4 institutions in 3 countries.
Funding
Abstract
A-type lamins are emerging as regulators of nuclear organization and function. Changes in their expression are associated with cancer and mutations are linked to degenerative diseases -laminopathies-. Although a correlation exists between alterations in lamins and genomic instability, the molecular mechanisms remain largely unknown. We previously found that loss of A-type lamins leads to degradation of 53BP1 protein and defective long-range non-homologous end-joining (NHEJ) of dysfunctional telomeres. Here, we determined how loss of A-type lamins affects the repair of short-range DNA double-strand breaks (DSBs) induced by ionizing radiation (IR). We find that lamins deficiency allows activation of the DNA damage response, but compromises the accumulation of 53BP1 at IR-induced foci (IRIF), hindering the fast phase of repair corresponding to classical-NHEJ. Importantly, reconstitution of 53BP1 is sufficient to rescue long-range and short-range NHEJ. Moreover, we demonstrate an unprecedented role for A-type lamins in the maintenance of homologous recombination (HR). Depletion of lamins compromises HR by a mechanism involving transcriptional downregulation of BRCA1 and RAD51 by the repressor complex formed by the Rb family member p130 and E2F4. In line with the DNA repair defects, lamins-deficient cells exhibit increased radiosensitivity. This study demonstrates that A-type lamins promote genomic stability by maintaining the levels of proteins with key roles in DNA DSBs repair by NHEJ and HR. Our results suggest that silencing of A-type lamins by DNA methylation in some cancers could contribute to the genomic instability that drives malignancy. In addition, lamins-deficient tumor cells could represent a good target for radiation therapy.
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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.