ArticleProceedings of the National Academy of Sciences of the United States of America2018
CHD4 and the NuRD complex directly control cardiac sarcomere formation.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 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
39 citing papers in PubMed, 68 citations in OpenAlex.
- CHD4 and NKX2.2 Cooperate to Regulate β-Cell Function by Repressing Non-β-Cell Gene Programs.Diabetes · 2026Article
- Conserved roles of GATA4 and its target gene TBX2 in regulation of human cardiogenesis.Biology open · 2026Article
- Epigenetic and chromatin remodeling mechanisms across cardiomyopathies: a comprehensive review.Epigenetics & chromatin · 2026Review
- Role of CHD chromatin remodelers in heart development.World journal of pediatrics : WJP · 2026Review
- Article
- Complex-specific HDAC1/2 regulation in the heart: insights from MiDAC disruption.American journal of physiology. Heart and circulatory physiology · 2026Article
- Review
- CHD4 and NKX2.2 Cooperate to Regulate Beta Cell Function by Repressing Non-Beta Cell Gene Programs.bioRxiv : the preprint server for biology · 2025Article
- The chromatin remodeler LET-418/Mi-2 regulates the intracellular pathogen response in the C. elegans intestine.BMC genomics · 2025Article
- TBX5 and CHD4 Coordinately Activate Atrial Cardiomyocyte Genes to Maintain Cardiac Rhythm Homeostasis.Circulation · 2025Article
- Review
- Generation and characterization of a mouse model of conditional Chd4 knockout in the endometrial epithelium.PloS one · 2025Article
- The molecular mechanisms of cardiac development and related diseases.Signal transduction and targeted therapy · 2024Review
- How does CHD4 slide nucleosomes?Biochemical Society transactions · 2024Review
- Genomic transcription factor binding site selection is edited by the chromatin remodeling factor CHD4.Nucleic acids research · 2024Article
- CHD4 and SMYD1 repress common transcriptional programs in the developing heart.Development (Cambridge, England) · 2024Article
- Human Genetics of Atrial Septal Defect.Advances in experimental medicine and biology · 2024Review
- Transcriptional derepression of CHD4/NuRD-regulated genes in the muscle of patients with dermatomyositis and anti-Mi2 autoantibodies.Annals of the rheumatic diseases · 2023Article
- Generation of a Well-Characterized Homozygous Chromodomain-Helicase-DNA-Binding Protein 4International journal of molecular sciences · 2023Article
- Missense Mutation in Human CHD4 Causes Ventricular Noncompaction by Repressing ADAMTS1.Circulation research · 2023Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Cardiac development relies on proper cardiomyocyte differentiation, including expression and assembly of cell-type-specific actomyosin subunits into a functional cardiac sarcomere. Control of this process involves not only promoting expression of cardiac sarcomere subunits but also repressing expression of noncardiac myofibril paralogs. This level of transcriptional control requires broadly expressed multiprotein machines that modify and remodel the chromatin landscape to restrict transcription machinery access. Prominent among these is the nucleosome remodeling and deacetylase (NuRD) complex, which includes the catalytic core subunit CHD4. Here, we demonstrate that direct CHD4-mediated repression of skeletal and smooth muscle myofibril isoforms is required for normal cardiac sarcomere formation, function, and embryonic survival early in gestation. Through transcriptomic and genome-wide analyses of CHD4 localization, we identified unique CHD4 binding sites in smooth muscle myosin heavy chain, fast skeletal α-actin, and the fast skeletal troponin complex genes. We further demonstrate that in the absence of CHD4, cardiomyocytes in the developing heart form a hybrid muscle cell that contains cardiac, skeletal, and smooth muscle myofibril components. These misexpressed paralogs intercalate into the nascent cardiac sarcomere to disrupt sarcomere formation and cause impaired cardiac function in utero. These results demonstrate the genomic and physiological requirements for CHD4 in mammalian cardiac development.
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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.