ArticleNucleic acids research2019
Lamin A/C promotes DNA base excision repair.
Article in Nucleic acids research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
What it found
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Who cites it
40 citing papers in PubMed, 56 citations in OpenAlex.
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- Integrating multiomics to elucidate the role of chromatin remodeling in glioma and the antitumor mechanisms and therapeutic potential of targeting LMNA.Frontiers in immunology · 2026Article
- Mechanosensitive snoRNA-like circular RNA sno-circCNOT1 drives endothelial dysfunction and atherosclerosis.Theranostics · 2026Article
- Selection of specific and efficient siRNAs in new cellular model for Hutchinson-Gilford progeria syndrome therapy.Molecular therapy. Nucleic acids · 2025Article
- LMNA-PRKDC axis enhances DNA repair and promotes chemoresistance in glioblastoma.Cell death & disease · 2025Article
- Cellular and Molecular Mechanisms of Oxidative DNA Damage and Repair.Medicina (Kaunas, Lithuania) · 2025Review
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- A genetic variant inScience advances · 2025Article
- Nuclear stiffness through lamin A/C overexpression differentially modulates chromosomal instability biomarkers.Biology of the cell · 2025Article
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- Mechanosensitive nuclear uptake of chemotherapy.Science advances · 2024Article
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- Progeria-based vascular model identifies networks associated with cardiovascular aging and disease.Aging cell · 2024Article
- NADNature cell biology · 2023Article
- The Molecular and Cellular Basis of Hutchinson-Gilford Progeria Syndrome and Potential Treatments.Genes · 2023Review
- Article
- The role of inner nuclear membrane proteins in tumourigenesis and as potential targets for cancer therapy.Cancer metastasis reviews · 2022Review
- The landscape of aging.Science China. Life sciences · 2022Review
- Possible Mechanisms of Resistance Development to Photodynamic Therapy (PDT) In Vulvar Cancer Cells.International journal of molecular sciences · 2022Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 3 countries.
Funding
Abstract
The A-type lamins (lamin A/C), encoded by the LMNA gene, are important structural components of the nuclear lamina. LMNA mutations lead to degenerative disorders known as laminopathies, including the premature aging disease Hutchinson-Gilford progeria syndrome. In addition, altered lamin A/C expression is found in various cancers. Reports indicate that lamin A/C plays a role in DNA double strand break repair, but a role in DNA base excision repair (BER) has not been described. We provide evidence for reduced BER efficiency in lamin A/C-depleted cells (Lmna null MEFs and lamin A/C-knockdown U2OS). The mechanism involves impairment of the APE1 and POLβ BER activities, partly effectuated by associated reduction in poly-ADP-ribose chain formation. Also, Lmna null MEFs displayed reduced expression of several core BER enzymes (PARP1, LIG3 and POLβ). Absence of Lmna led to accumulation of 8-oxoguanine (8-oxoG) lesions, and to an increased frequency of substitution mutations induced by chronic oxidative stress including GC>TA transversions (a fingerprint of 8-oxoG:A mismatches). Collectively, our results provide novel insights into the functional interplay between the nuclear lamina and cellular defenses against oxidative DNA damage, with implications for cancer and aging.
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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.