ReviewNucleus (Austin, Tex.)2018
Causes and consequences of genomic instability in laminopathies: Replication stress and interferon response.
Review in Nucleus (Austin, Tex.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
What it found
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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
47 citing papers in PubMed, 66 citations in OpenAlex.
- Lamins gate nuclear and chromatin structures for cardiomyocyte maturation genes.bioRxiv : the preprint server for biology · 2026Article
- 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
- CHK1 is an integral regulator of DNA replication in human cells.Cell death & disease · 2026Article
- Computational Characterization of Pathogenic LMNA Missense Variants: Structural Instability, Altered Binding, and Conformational Dynamics.Human mutation · 2026Article
- Sterile inflammation in laminopathies.European journal of cell biology · 2025Review
- Closing the loops: chromatin loop dynamics after DNA damage.Nucleus (Austin, Tex.) · 2025Review
- 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
- Nuclear compression-mediated DNA damage drives ATR-dependent Lamin expression and mouse ESC differentiation.Nucleic acids 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
- Cyclin E1 overexpression triggers interferon signaling and is associated with antitumor immunity in breast cancer.Journal for immunotherapy of cancer · 2025Article
- The synergistic effect of c-Myb hyperactivation and Pu.1 deficiency induces Pelger-Huët anomaly and promotes sAML.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- The transmembrane protein Syndecan is required for stem cell survival and maintenance of their nuclear properties.PLoS genetics · 2025Article
- The triple code model for advancing research in rare and undiagnosed diseases beyond the base pairs.Epigenomics · 2025Article
- Regulation of TAR DNA binding protein 43 (TDP-43) homeostasis by cytosolic DNA accumulation.The Journal of biological chemistry · 2024Article
- A Youthful Touch: Reversal of Aging Hallmarks by Cell Reprogramming.Cells, tissues, organs · 2024Review
- Lamin A/C facilitates DNA damage response by modulating ATM signaling and homologous recombination pathways.Animal cells and systems · 2024Article
- DNA replication and replication stress response in the context of nuclear architecture.Chromosoma · 2024Review
- Regulation of cellular senescence by innate immunity.Biophysics reports · 2023Article
- Model Systems to Study the Mechanism of Vascular Aging.International journal of molecular sciences · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Mammalian nuclei are equipped with a framework of intermediate filaments that function as a karyoskeleton. This nuclear scaffold, formed primarily by lamins (A-type and B-type), maintains the spatial and functional organization of the genome and of sub-nuclear compartments. Over the past decade, a body of evidence has highlighted the significance of these structural nuclear proteins in the maintenance of nuclear architecture and mechanical stability, as well as genome function and integrity. The importance of these structures is now unquestioned given the wide range of degenerative diseases that stem from LMNA gene mutations, including muscular dystrophy disorders, peripheral neuropathies, lipodystrophies, and premature aging syndromes. Here, we review our knowledge about how alterations in nuclear lamins, either by mutation or reduced expression, impact cellular mechanisms that maintain genome integrity. Despite the fact that DNA replication is the major source of DNA damage and genomic instability in dividing cells, how alterations in lamins function impact replication remains minimally explored. We summarize recent studies showing that lamins play a role in DNA replication, and that the DNA damage that accumulates upon lamins dysfunction is elicited in part by deprotection of replication forks. We also discuss the emerging model that DNA damage and replication stress are "sensed" at the cytoplasm by proteins that normally survey this space in search of foreign nucleic acids. In turn, these cytosolic sensors activate innate immune responses, which are materializing as important players in aging and cancer, as well as in the response to cancer immunotherapy.
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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.