ArticleProceedings of the National Academy of Sciences of the United States of America2010
Nonmuscle myosin II isoform and domain specificity during early mouse development.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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Who cites it
58 citing papers in PubMed, 87 citations in OpenAlex.
- MYH9 mutations differentially stabilize non-muscle myosin II filaments and induce distinct cellular aggregation phenotypes.Cellular and molecular life sciences : CMLS · 2026Article
- Intravital single-molecule imaging reveals cytoskeletal turnover as a driver of membrane remodeling in live animals.bioRxiv : the preprint server for biology · 2026Article
- Neurogranin-MYH9 interaction regulates cytoskeletal remodeling in cerebral vasculature.Fluids and barriers of the CNS · 2025Article
- Cisplatin-Induced APE2 Overexpression Disrupts MYH9 Function and Causes Hearing Loss.Cancer research communications · 2025Article
- Mechanisms of Homoarginine: Looking Beyond Clinical Outcomes.Acta physiologica (Oxford, England) · 2025Review
- Endothelial Myosin IIA Is Required for the Maintenance of Blood-Brain Barrier Integrity.Cells · 2024Article
- Non-Muscle Myosin II A: Friend or Foe in Cancer?International journal of molecular sciences · 2024Review
- Structure, regulation, and mechanisms of nonmuscle myosin-2.Cellular and molecular life sciences : CMLS · 2024Review
- Myosin II mediates Shh signals to shape dental epithelia via control of cell adhesion and movement.PLoS genetics · 2024Article
- Non-muscle myosin 2 at a glance.Journal of cell science · 2023Review
- Non-muscle myosins control radial glial basal endfeet to mediate interneuron organization.PLoS biology · 2023Article
- Unique and redundant functions of cytoplasmic actins and nonmuscle myosin II isoforms at epithelial junctions.Annals of the New York Academy of Sciences · 2022Review
- Forces in stem cells and cancer stem cells.Cells & development · 2022Review
- Scribble mutation disrupts convergent extension and apical constriction during mammalian neural tube closure.Developmental biology · 2021Article
- Akt1-associated actomyosin remodelling is required for nuclear lamina dispersal and nuclear shrinkage in epidermal terminal differentiation.Cell death and differentiation · 2021Article
- Endothelial cell invasion is controlled by dactylopodia.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Article
- Non-muscle myosin II regulates aortic stiffness through effects on specific focal adhesion proteins and the non-muscle cortical cytoskeleton.Journal of cellular and molecular medicine · 2021Article
- Cisplatin-Mediated Upregulation of APE2 Binding to MYH9 Provokes Mitochondrial Fragmentation and Acute Kidney Injury.Cancer research · 2021Article
- Mutations in non-muscle myosin 2A disrupt the actomyosin cytoskeleton in Sertoli cells and cause male infertility.Developmental biology · 2021Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Nonmuscle myosins (NMs) II-A and II-B are essential for embryonic mouse development, but their specific roles are not completely defined. Here we examine the isoforms and their domain specifically in vivo and in vitro by studying mice and cells in which nonmuscle myosin heavy chain (NMHC) II-A is genetically replaced by NMHC II-B or chimeric NMHC IIs that exchange the rod and head domains of NM II-A and II-B. In contrast with the failure of visceral endoderm formation resulting in embryonic day (E)6.5 lethality of A(-)/A(-) mice, replacement with NM II-B or chimeric NM IIs restores a normal visceral endoderm. This finding is consistent with NM II's role in cell adhesion and also confirms an essential, isoform-independent requirement for NM II in visceral endoderm function. The knock-in mice die between E9.5 and 12.5 because of defects in placenta formation associated with abnormal angiogenesis and cell migration, revealing a unique function for NM II-A in placenta development. In vitro results further support a requirement for NM II-A in directed cell migration and focal adhesion formation. These findings demonstrate an isoform-specific role for NM II-A during these processes, making replacement by another isoform, or chimeric NM II isoforms, less successful. The failure of these substitutions is not only related to the different kinetic properties of NM II-A and II-B, but also to their subcellular localization determined by the C-terminal domain. These results highlight the functions of the N-terminal motor and C-terminal rod domains of NM II and their different roles in cell-cell and cell-matrix adhesion.
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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.