ArticleChromosoma2012
Mapping of lamin A- and progerin-interacting genome regions.
Article in Chromosoma, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 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.
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Who cites it
52 citing papers in PubMed, 91 citations in OpenAlex.
- LATS1/2-CD38 Metabolic Rewiring Links Senescence to Intraplaque Thrombosis.Circulation research · 2026Article
- B-type lamins maintain transcriptional homeostasis by spatially controlling chromatin-speckle proximity.Nucleic acids research · 2026Article
- The dual guardians of cellular stability: exploring nesprin and lamin in senescence.Cell death & disease · 2025Review
- Chromatin phase separation and nuclear shape fluctuations are correlated in a polymer model of the nucleus.Nucleus (Austin, Tex.) · 2024Article
- Alterations to Genome Organisation in Stem Cells, Their Differentiation and Associated Diseases.Results and problems in cell differentiation · 2022Article
- Self-assembly of multi-component mitochondrial nucleoids via phase separation.The EMBO journal · 2021Article
- Three-dimensional chromatin organization in cardiac development and disease.Journal of molecular and cellular cardiology · 2021Review
- A Unified Linear Viscoelastic Model of the Cell Nucleus Defines the Mechanical Contributions of Lamins and Chromatin.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2020Article
- The Histone Code of Senescence.Cells · 2020Review
- Telomere elongation through hTERT immortalization leads to chromosome repositioning in control cells and genomic instability in Hutchinson-Gilford progeria syndrome fibroblasts, expressing a novel SUN1 isoform.Genes, chromosomes & cancer · 2019Article
- Genomic Reorganization of Lamin-Associated Domains in Cardiac Myocytes Is Associated With Differential Gene Expression and DNA Methylation in Human Dilated Cardiomyopathy.Circulation research · 2019Article
- HiPLA: High-throughput imaging proximity ligation assay.Methods (San Diego, Calif.) · 2019Article
- Hutchinson-Gilford Progeria Syndrome-Current Status and Prospects for Gene Therapy Treatment.Cells · 2019Review
- Farnesyltransferase inhibitor and rapamycin correct aberrant genome organisation and decrease DNA damage respectively, in Hutchinson-Gilford progeria syndrome fibroblasts.Biogerontology · 2018Article
- Chromatin histone modifications and rigidity affect nuclear morphology independent of lamins.Molecular biology of the cell · 2018Article
- Protein sequestration at the nuclear periphery as a potential regulatory mechanism in premature aging.The Journal of cell biology · 2018Review
- CELL FATE DETERMINATION IN 3D: REGULATION OF GENE EXPRESSION VIA CHROMATIN INTERACTIONS WITH THE NUCLEAR MEMBRANE.Transactions of the American Clinical and Climatological Association · 2018Article
- An overview of treatment strategies for Hutchinson-Gilford Progeria syndrome.Nucleus (Austin, Tex.) · 2018Review
- Article
- Identification of novel RNA isoforms of LMNA.Nucleus (Austin, Tex.) · 2017Article
Corrections and comments
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Authors and funding
6 authors at 6 institutions in 2 countries.
Funding
Abstract
Mutations in the A-type lamins A and C, two major components of the nuclear lamina, cause a large group of phenotypically diverse diseases collectively referred to as laminopathies. These conditions often involve defects in chromatin organization. However, it is unclear whether A-type lamins interact with chromatin in vivo and whether aberrant chromatin-lamin interactions contribute to disease. Here, we have used an unbiased approach to comparatively map genome-wide interactions of gene promoters with lamin A and progerin, the mutated lamin A isoform responsible for the premature aging disorder Hutchinson-Gilford progeria syndrome (HGPS) in mouse cardiac myoytes and embryonic fibroblasts. We find that lamin A-associated genes are predominantly transcriptionally silent and that loss of lamin association leads to the relocation of peripherally localized genes, but not necessarily to their activation. We demonstrate that progerin induces global changes in chromatin organization by enhancing interactions with a specific subset of genes in addition to the identified lamin A-associated genes. These observations demonstrate disease-related changes in higher order genome organization in HGPS and provide novel insights into the role of lamin-chromatin interactions in chromatin 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.