ArticleMolecular biology of the cell2017
Differential role of nonmuscle myosin II isoforms during blebbing of MCF-7 cells.
Article in Molecular biology of the cell, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Cellular elasticity drives mechano-adaptation against fluid shear stress.Journal of cell science · 2025Article
- Alteration of the Expression and Functional Activities of Myosin II Isoforms in Enlarged Hyperplastic Prostates.Journal of personalized medicine · 2024Article
- Investigation of the effects of downregulation of jumping translocation breakpoint (JTB) protein expression in MCF7 cells for potential use as a biomarker in breast cancer.American journal of cancer research · 2022Article
- Nonmuscle myosin IIA and IIB differentially modulate migration and alter gene expression in primary mouse tumorigenic cells.Molecular biology of the cell · 2019Article
- Common and Specific Functions of Nonmuscle Myosin II Paralogs in Cells.Biochemistry. Biokhimiia · 2018Review
- Mammalian nonmuscle myosin II comes in three flavors.Biochemical and biophysical research communications · 2018Review
- Ultrastructure of the actin cytoskeleton.Current opinion in cell biology · 2018Review
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Authors and funding
9 authors.
Funding
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Abstract
Bleb formation has been correlated with nonmuscle myosin II (NM-II) activity. Whether three isoforms of NM-II (NM-IIA, -IIB and -IIC) have the same or differential roles in bleb formation is not well understood. Here we report that ectopically expressed, GFP-tagged NM-II isoforms exhibit different types of membrane protrusions, such as multiple blebs, lamellipodia, combinations of both, or absence of any such protrusions in MCF-7 cells. Quantification suggests that 50% of NM-IIA-GFP-, 29% of NM-IIB-GFP-, and 19% of NM-IIC1-GFP-expressing MCF-7 cells show multiple bleb formation, compared with 36% of cells expressing GFP alone. Of interest, NM-IIB has an almost 50% lower rate of dissociation from actin filament than NM-IIA and -IIC1 as determined by FRET analysis both at cell and bleb cortices. We induced bleb formation by disruption of the cortex and found that all three NM-II-GFP isoforms can reappear and form filaments but to different degrees in the growing bleb. NM-IIB-GFP can form filaments in blebs in 41% of NM-IIB-GFP-expressing cells, whereas filaments form in only 12 and 3% of cells expressing NM-IIA-GFP and NM-IIC1-GFP, respectively. These studies suggest that NM-II isoforms have differential roles in the bleb life cycle.
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