ArticlePLoS genetics2017
Non-muscle myosin IIB (Myh10) is required for epicardial function and coronary vessel formation during mammalian development.
Article in PLoS genetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
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Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.
- Genome-wide interaction study with major depression identifies novel variants associated with cognitive function.Molecular psychiatry · 2022Pooled it
- RNF126 mediates fetal growth restriction via ubiquitination-dependent degradation of the MYH9/MYH10 complex.iScience · 2026Article
- A machine learning classifier to identify and prioritise genes associated with murine cardiac development.PLoS genetics · 2026Article
- Broadening horizons: new links between cilia and heart development and disease.Frontiers in cardiovascular medicine · 2026Review
- The RNA splicing factor PRPF8 is required for left-right organiser cilia differentiation and determination of cardiac left-right asymmetry via regulation ofbioRxiv : the preprint server for biology · 2025Article
- A Novel Disulfidptosis-Related Diagnostic Gene Signature and Differential Expression Validation in Ischaemic Cardiomyopathy.Journal of cellular and molecular medicine · 2025Article
- Epicardium-myocardium crosstalk orchestrates heart development.Frontiers in cell and developmental biology · 2025Review
- Epicardial EMT and cardiac repair: an update.Stem cell research & therapy · 2024Review
- Deficiency in Prader-Willi syndrome geneiScience · 2024Article
- Congenital Coronary Blood Vessel Anomalies: Animal Models and the Integration of Developmental Mechanisms.Advances in experimental medicine and biology · 2024Article
- Functions of cilia in cardiac development and disease.Annals of human genetics · 2024Review
- MARVEL: an integrated alternative splicing analysis platform for single-cell RNA sequencing data.Nucleic acids research · 2023Article
- Differential Expression of microRNAs in Serum of Patients with Chronic Painful Polyneuropathy and Healthy Age-Matched Controls.Biomedicines · 2023Article
- Scalable Generation of Nanovesicles from Human-Induced Pluripotent Stem Cells for Cardiac Repair.International journal of molecular sciences · 2022Article
- Down-regulation of MYH10 driven by chromosome 17p13.1 deletion promotes hepatocellular carcinoma metastasis through activation of the EGFR pathway.Journal of cellular and molecular medicine · 2021Article
- Developmental lineage of human pluripotent stem cell-derived cardiac fibroblasts affects their functional phenotype.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- miR-29c&b2 encourage extramedullary infiltration resulting in the poor prognosis of acute myeloid leukemia.Oncogene · 2021Article
- The transcriptome of anterior regeneration in earthworm Eudrilus eugeniae.Molecular biology reports · 2021Article
- Collagen, stiffness, and adhesion: the evolutionary basis of vertebrate mechanobiology.Molecular biology of the cell · 2020Review
- Myosin II isoforms play distinct roles ineLife · 2019Article
Corrections and comments
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Authors and funding
17 authors at 3 institutions in 1 country.
Funding
Abstract
The coronary vasculature is an essential vessel network providing the blood supply to the heart. Disruptions in coronary blood flow contribute to cardiac disease, a major cause of premature death worldwide. The generation of treatments for cardiovascular disease will be aided by a deeper understanding of the developmental processes that underpin coronary vessel formation. From an ENU mutagenesis screen, we have isolated a mouse mutant displaying embryonic hydrocephalus and cardiac defects (EHC). Positional cloning and candidate gene analysis revealed that the EHC phenotype results from a point mutation in a splice donor site of the Myh10 gene, which encodes NMHC IIB. Complementation testing confirmed that the Myh10 mutation causes the EHC phenotype. Characterisation of the EHC cardiac defects revealed abnormalities in myocardial development, consistent with observations from previously generated NMHC IIB null mouse lines. Analysis of the EHC mutant hearts also identified defects in the formation of the coronary vasculature. We attribute the coronary vessel abnormalities to defective epicardial cell function, as the EHC epicardium displays an abnormal cell morphology, reduced capacity to undergo epithelial-mesenchymal transition (EMT), and impaired migration of epicardial-derived cells (EPDCs) into the myocardium. Our studies on the EHC mutant demonstrate a requirement for NMHC IIB in epicardial function and coronary vessel formation, highlighting the importance of this protein in cardiac development and ultimately, embryonic survival.
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Registered trials
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