ArticleThe Journal of cell biology2019
Chromatin compartment dynamics in a haploinsufficient model of cardiac laminopathy.
Article in The Journal of cell biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 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
49 citing papers in PubMed, 70 citations in OpenAlex.
- The cardiac 4D nucleome: nuclear and chromatin dynamics across development, disease and ageing.Nature reviews. Cardiology · 2026Review
- Review
- The cytoskeleton contributes to abnormal genome-lamina interactions in LMNA-deficient cardiomyocytes.The Journal of cell biology · 2026Article
- Epigenetics, Modifiers, and Molecular Noise: Rethinking Pathophysiology in Dilated and Hypertrophic Cardiomyopathies.International journal of molecular sciences · 2026Review
- An epigenomic investigation of atrial fibrillation in a matched left and right atrial human cohort.Clinical epigenetics · 2026Article
- Lamin A/C-regulated cysteine catabolic flux modulates stem cell fate through epigenome reprogramming.Nature metabolism · 2026Article
- Single cell transcriptional perturbome in pluripotent stem cell models.Molecular systems biology · 2026Article
- Epigenetic Regulation in Dilated Cardiomyopathy.Heart failure clinics · 2026Review
- LMNA-related cardiomyopathy: From molecular pathology to cardiac gene therapy.Journal of advanced research · 2025Review
- Microtubule forces drive nuclear damage in LMNA cardiomyopathy.Nature cardiovascular research · 2025Article
- MAM-STAT3-Driven Mitochondrial CaAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Discovery of therapeutic targets in cardiovascular diseases using high-throughput chromosome conformation capture (Hi-C).Frontiers in genetics · 2025Review
- Role of Nuclear Lamins in the Regulation of the Genome: Focus on CardioLaminopathy.Sub-cellular biochemistry · 2025Review
- Article
- Chromosome compartmentalization: causes, changes, consequences, and conundrums.Trends in cell biology · 2024Review
- Lamin A/C deficiency-mediated ROS elevation contributes to pathogenic phenotypes of dilated cardiomyopathy in iPSC model.Nature communications · 2024Article
- PIGB maintains nuclear lamina organization in skeletal muscle of Drosophila.The Journal of cell biology · 2024Article
- Epigenetics.Advances in experimental medicine and biology · 2024Review
- Interdependent changes of nuclear lamins, nuclear pore complexes, and ploidy regulate cellular regeneration and stress response in the heart.Nucleus (Austin, Tex.) · 2023Review
- Nuclear damage inMolecular biology of the cell · 2023Article
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
Abstract
Mutations in A-type nuclear lamins cause dilated cardiomyopathy, which is postulated to result from dysregulated gene expression due to changes in chromatin organization into active and inactive compartments. To test this, we performed genome-wide chromosome conformation analyses in human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) with a haploinsufficient mutation for lamin A/C. Compared with gene-corrected cells, mutant hiPSC-CMs have marked electrophysiological and contractile alterations, with modest gene expression changes. While large-scale changes in chromosomal topology are evident, differences in chromatin compartmentalization are limited to a few hotspots that escape segregation to the nuclear lamina and inactivation during cardiogenesis. These regions exhibit up-regulation of multiple noncardiac genes including
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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.