ArticleProceedings of the National Academy of Sciences of the United States of America2012
Regulation of prelamin A but not lamin C by miR-9, a brain-specific microRNA.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 128 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
128 citing papers in PubMed, 1 synthesis or guideline pooled it, 220 citations in OpenAlex.
- Mechanosensing by the nucleus: From pathways to scaling relationships.The Journal of cell biology · 2017Pooled it
- Article
- Expression of progerin enhances disease-related endpoints in a tau seeding reporter cell system.GeroScience · 2026Article
- IVNS1ABP mutation drives cellular senescence in newly identified progeroid neuropathy.Nature communications · 2026Article
- Roles of DNA Damage Response Pathway in the Regulation of the Nuclear Envelope.Current issues in molecular biology · 2026Review
- Dynamic expression of lamin B1 during adult neurogenesis in the vertebrate brain.Developmental dynamics : an official publication of the American Association of Anatomists · 2026Article
- Article
- Unraveling the mysteries of Hutchinson-Gilford progeria syndrome: a comprehensive review of LMNA gene mutations.Biogerontology · 2025Review
- Patient-Derived Cortical Organoids Reveal Senescence of Neural Progenitor Cells in Hutchinson-Gilford Progeria Syndrome.Aging cell · 2025Article
- miR-548t-3p impairs nuclear mechanosensitivity and focal adhesion via lamin A/C downregulation.Biophysical journal · 2025Article
- Lamin A/C regulates cerebellar granule cell maturation.Cell biology and toxicology · 2025Article
- Article
- Decreasing Lamin A Triggers Cell Fate Transitions through Heterochromatin-Nuclear Periphery Detethering.Biomaterials research · 2025Article
- Disorganized chromatin hierarchy and stem cell aging in a male patient of atypical laminopathy-based progeria mandibuloacral dysplasia type A.Nature communications · 2024Article
- Progerin mRNA expression in non-HGPS patients is correlated with widespread shifts in transcript isoforms.NAR genomics and bioinformatics · 2024Article
- Navigating Lipodystrophy: Insights from Laminopathies and Beyond.International journal of molecular sciences · 2024Review
- Targeting Cellular Senescence in Aging and Age-Related Diseases: Challenges, Considerations, and the Emerging Role of Senolytic and Senomorphic Therapies.Aging and disease · 2024Review
- Review
- Discovery of a Small-Molecule Modulator of the Autophagy-Lysosome Pathway That Targets Lamin A/C and LAMP1, Induces Autophagic Flux, and Affects Lysosome Positioning in Neurons.ACS chemical neuroscience · 2023Article
- Nuclear lamin facilitates collective border cell invasion into confined spaces in vivo.The Journal of cell biology · 2023Article
68 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
12 authors at 3 institutions in 1 country.
Funding
Abstract
Lamins A and C, alternatively spliced products of the LMNA gene, are key components of the nuclear lamina. The two isoforms are found in similar amounts in most tissues, but we observed an unexpected pattern of expression in the brain. Western blot and immunohistochemistry studies showed that lamin C is abundant in the mouse brain, whereas lamin A and its precursor prelamin A are restricted to endothelial cells and meningeal cells and are absent in neurons and glia. Prelamin A transcript levels were low in the brain, but this finding could not be explained by alternative splicing. In lamin A-only knockin mice, where alternative splicing is absent and all the output of the gene is channeled into prelamin A transcripts, large amounts of lamin A were found in peripheral tissues, but there was very little lamin A in the brain. Also, in knockin mice expressing exclusively progerin (a toxic form of prelamin A found in Hutchinson-Gilford progeria syndrome), the levels of progerin in the brain were extremely low. Further studies showed that prelamin A expression, but not lamin C expression, is down-regulated by a brain-specific microRNA, miR-9. Expression of miR-9 in cultured cells reduced lamin A expression, and this effect was abolished when the miR-9-binding site in the prelamin A 3' UTR was mutated. The down-regulation of prelamin A expression in the brain could explain why mouse models of Hutchinson-Gilford progeria syndrome are free of central nervous system pathology.
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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.