ArticleDevelopmental dynamics : an official publication of the American Association of Anatomists2021
DZIP1 regulates mammalian cardiac valve development through a Cby1-β-catenin mechanism.
Article in Developmental dynamics : an official publication of the American Association of Anatomists, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- Mechanisms of mitral valve development and disease.Frontiers in cardiovascular medicine · 2026Review
- Connective tissue disorders and cardiac arrhythmias: genetic pathways, mechanistic bridges, and clinical implications.Frontiers in cardiovascular medicine · 2026Review
- Broadening horizons: new links between cilia and heart development and disease.Frontiers in cardiovascular medicine · 2026Review
- Article
- The Potential of Intertwining Gene Diagnostics and Surgery for Mitral Valve Prolapse.Journal of clinical medicine · 2023Review
- Genetics and pathophysiology of mitral valve prolapse.Frontiers in cardiovascular medicine · 2023Review
- DCHS1, Lix1L, and the Septin Cytoskeleton: Molecular and Developmental Etiology of Mitral Valve Prolapse.Journal of cardiovascular development and disease · 2022Article
- DZIP1 regulates mammalian cardiac valve development through a Cby1-β-catenin mechanism.Developmental dynamics : an official publication of the American Association of Anatomists · 2021Article
Corrections and comments
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Authors and funding
14 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundMitral valve prolapse (MVP) is a common and progressive cardiovascular disease with developmental origins. How developmental errors contribute to disease pathogenesis are not well understood.
resultsA multimeric complex was identified that consists of the MVP gene Dzip1, Cby1, and β-catenin. Co-expression during valve development revealed overlap at the basal body of the primary cilia. Biochemical studies revealed a DZIP1 peptide required for stabilization of the complex and suppression of β-catenin activities. Decoy peptides generated against this interaction motif altered nuclear vs cytosolic levels of β-catenin with effects on transcriptional activity. A mutation within this domain was identified in a family with inherited non-syndromic MVP. This novel mutation and our previously identified DZIP1
conclusionDzip1 functions to restrain β-catenin signaling through a CBY1 linker during cardiac development. Loss of these interactions results in increased nuclear β-catenin/Lef1 and excess MMP2 production, which correlates with developmental and postnatal changes in ECM and generation of a myxomatous phenotype.
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