ArticleNature communications2024
The chromatin regulator Ankrd11 controls cardiac neural crest cell-mediated outflow tract remodeling and heart function.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- ANKRD11 deficiency reprograms CD8Nature immunology · 2026Article
- [Research progress on the regulatory role and mechanisms of the Hippo signaling pathway in the pathogenesis of congenital heart disease].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2026Review
- Role of CHD chromatin remodelers in heart development.World journal of pediatrics : WJP · 2026Review
- ANKRD53 is downregulated in human obesity and coordinates lipolysis with mitochondrial oxidative metabolism in adipocytes.Molecular metabolism · 2026Article
- ANKRD1 sustains a neurogenic BMSC niche and counters cognitive aging.International journal of oral science · 2026Article
- NovelSultan Qaboos University medical journal · 2026Article
- Uric Acid Disrupts Heart Development in Zebrafish by Inhibiting the Wnt Signaling Pathway.Cardiovascular toxicology · 2025Article
- ANKRD11 binding to cohesin suggests a connection between KBG syndrome and Cornelia de Lange syndrome.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Post-translational modifications orchestrate mTOR-driven cell death in cardiovascular disease.Frontiers in cardiovascular medicine · 2025Review
- Insights into the ANKRD11 variants and short-stature phenotype through literature review and ClinVar database search.Orphanet journal of rare diseases · 2024Review
- The chromatin regulator Ankrd11 controls cardiac neural crest cell-mediated outflow tract remodeling and heart function.Nature communications · 2024Article
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Authors and funding
16 authors.
Funding
Abstract
ANKRD11 (Ankyrin Repeat Domain 11) is a chromatin regulator and a causative gene for KBG syndrome, a rare developmental disorder characterized by multiple organ abnormalities, including cardiac defects. However, the role of ANKRD11 in heart development is unknown. The neural crest plays a leading role in embryonic heart development, and its dysfunction is implicated in congenital heart defects. We demonstrate that conditional knockout of Ankrd11 in the murine embryonic neural crest results in persistent truncus arteriosus, ventricular dilation, and impaired ventricular contractility. We further show these defects occur due to aberrant cardiac neural crest cell organization leading to outflow tract septation failure. Lastly, knockout of Ankrd11 in the neural crest leads to impaired expression of various transcription factors, chromatin remodelers and signaling pathways, including mTOR, BMP and TGF-β in the cardiac neural crest cells. In this work, we identify Ankrd11 as a regulator of neural crest-mediated heart development and function.
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