ArticleDevelopmental cell2020
Phosphorylated Lamin A/C in the Nuclear Interior Binds Active Enhancers Associated with Abnormal Transcription in Progeria.
Article in Developmental cell, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.
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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
74 citing papers in PubMed, 113 citations in OpenAlex.
- Lack of evidence for transcription-to-RNA maturation lags across G1-to-G2-phase boundary in fibroblasts.Life science alliance · 2026Article
- Extracellular matrix abnormalities in Hutchinson-Gilford progeria fibroblasts: a specific defect in collagen IV and basement membrane architecture?Matrix biology plus · 2026Article
- Orientia tsutsugamushi targets lamin A using Ank effectors and alters chromatin to inhibit NF-κB.Communications biology · 2026Article
- Lamin A/C as a Molecular Link Between Nuclear Organization, Chromatin Dynamics, and Tumor Progression.Cells · 2026Review
- MMP-3 cleavage of Lamin A induces pro-migratory nuclear deformity, nucleophagy, and their autophagic secretion with extracellular vesicles in metastatic cancer.Cell communication and signaling : CCS · 2026Article
- Phosphorylation-dependent modulation of the Lamin A/C-EZH2 complex regulates epithelial-mesenchymal plasticity.Nucleic acids research · 2026Article
- Mechanosensitive snoRNA-like circular RNA sno-circCNOT1 drives endothelial dysfunction and atherosclerosis.Theranostics · 2026Article
- Vascular Mechanobiology: From Membrane to Nucleus.Advances in experimental medicine and biology · 2026Review
- Nuclear envelope and chromatin choreography direct cellular differentiation.Nucleus (Austin, Tex.) · 2025Review
- Mitotic DNA repair by TMEJ suppresses replication stress-induced nuclear envelope reassembly defect.Nature communications · 2025Article
- The molecular basis of lamin-specific chromatin interactions.Nature structural & molecular biology · 2025Article
- Article
- Cell-cycle dynamics of nascent transcription and mature RNA accumulation are concordant in normal fibroblasts.bioRxiv : the preprint server for biology · 2025Article
- Lamin B1 and LAP2β resist cytoskeletal force to maintain lamin A/C meshwork organization and preserve nuclear integrity.Molecular biology of the cell · 2025Article
- Cryosectioning-enhanced super-resolution microscopy for single-protein imaging across cells and tissues.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- A SETD2-CDK1-lamin axis maintains nuclear morphology and genome stability.Nature cell biology · 2025Article
- Starvation activates ECM-remodeling gene transcription and putative enhancers in fibroblasts despite inducing quiescence.Cell reports · 2025Article
- High matrix stiffness promotes senescence of type II alveolar epithelial cells by lysosomal degradation of lamin A/C in pulmonary fibrosis.Respiratory research · 2025Article
- Feeling the force from within - new tools and insights into nuclear mechanotransduction.Journal of cell science · 2025Review
- Role of Nuclear Lamins in the Regulation of the Genome: Focus on CardioLaminopathy.Sub-cellular biochemistry · 2025Review
14 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
LMNA encodes nuclear Lamin A/C that tethers lamina-associated domains (LADs) to the nuclear periphery. Mutations in LMNA cause degenerative disorders including the premature aging disorder Hutchinson-Gilford progeria, but the mechanisms are unknown. We report that Ser22-phosphorylated (pS22) Lamin A/C was localized to the nuclear interior in human fibroblasts throughout the cell cycle. pS22-Lamin A/C interacted with a subset of putative active enhancers, not LADs, at locations co-bound by the transcriptional activator c-Jun. In progeria-patient fibroblasts, a subset of pS22-Lamin A/C-binding sites were lost, whereas new pS22-Lamin A/C-binding sites emerged in normally quiescent loci. New pS22-Lamin A/C binding was accompanied by increased histone acetylation, increased c-Jun binding, and upregulation of nearby genes implicated in progeria pathophysiology. These results suggest that Lamin A/C regulates gene expression by enhancer binding. Disruption of the gene regulatory rather than LAD tethering function of Lamin A/C may underlie the pathogenesis of disorders caused by LMNA mutations.
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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.