ArticlePloS one2013
A-type lamins maintain the positional stability of DNA damage repair foci in mammalian nuclei.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.
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Who cites it
33 citing papers in PubMed, 1 synthesis or guideline pooled it, 58 citations in OpenAlex.
- Biomarkers of tumor invasiveness in proteomics (Review).International journal of oncology · 2020Pooled it
- Navigating the cancer cell nucleus: lamins at the interface of epigenetic regulation and tumorigenesis.Molecular biology reports · 2026Review
- A nucleoskeleton network preserves genomic integrity by promoting NHEJ and restraining chromosome translocations.Nucleic acids research · 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
- Radiation symptoms resemble laminopathies and the physical underlying cause may sit at the lamin A C-terminus.Molecular medicine (Cambridge, Mass.) · 2025Article
- Lamin A/C facilitates DNA damage response by modulating ATM signaling and homologous recombination pathways.Animal cells and systems · 2024Article
- Simulating Space Conditions Evokes Different DNA Damage Responses in Immature and Mature Cells of the Human Hematopoietic System.International journal of molecular sciences · 2023Article
- Article
- Lamin B1 sequesters 53BP1 to control its recruitment to DNA damage.Science advances · 2021Article
- Review
- Article
- The nucleoskeleton protein IFFO1 immobilizes broken DNA and suppresses chromosome translocation during tumorigenesis.Nature cell biology · 2019Article
- Review
- HiPLA: High-throughput imaging proximity ligation assay.Methods (San Diego, Calif.) · 2019Article
- Lamins in Lung Cancer: Biomarkers and Key Factors for Disease Progression through miR-9 Regulation?Cells · 2018Review
- Random Motion of Chromatin Is Influenced by Lamin A Interconnections.Biophysical journal · 2018Article
- The Pathogenesis and Therapies of Striated Muscle Laminopathies.Frontiers in physiology · 2018Review
- Lamin B2 Modulates Nucleolar Morphology, Dynamics, and Function.Molecular and cellular biology · 2017Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
A-type lamins encoded by LMNA form a structural fibrillar meshwork within the mammalian nucleus. How this nuclear organization may influence the execution of biological processes involving DNA transactions remains unclear. Here, we characterize changes in the dynamics and biochemical interactions of lamin A/C after DNA damage. We find that DNA breakage reduces the mobility of nucleoplasmic GFP-lamin A throughout the nucleus as measured by dynamic fluorescence imaging and spectroscopy in living cells, suggestive of incorporation into stable macromolecular complexes, but does not induce the focal accumulation of GFP-lamin A at damage sites. Using a proximity ligation assay and biochemical analyses, we show that lamin A engages chromatin via histone H2AX and its phosphorylated form (γH2AX) induced by DNA damage, and that these interactions are enhanced after DNA damage. Finally, we use three-dimensional time-lapse imaging to show that LMNA inactivation significantly reduces the positional stability of DNA repair foci in living cells. This defect is partially rescued by the stable expression of GFP-lamin A. Thus collectively, our findings suggest that the dynamic structural meshwork formed by A-type lamins anchors sites of DNA repair in mammalian nuclei, providing fresh insight into the control of DNA transactions by nuclear structural organization.
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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.