ArticleBiology open2018
Nonmuscle myosin IIA is involved in recruitment of apical junction components through activation of α-catenin.
Article in Biology open, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
18 citing papers in PubMed, 25 citations in OpenAlex.
- Nonmuscle myosin IIA (NMIIA) regulates anisotropic cell tension to maintain the hexagonal packing of mouse lens meridional row cells.Molecular biology of the cell · 2025Article
- Regulation of epithelial cell jamming transition by cytoskeleton and cell-cell interactions.Biophysics reviews · 2024Review
- Loss of Cell-Cell Contact Inhibits Cellular Differentiation of α-Catenin Knock Out P19 Embryonal Carcinoma Cells and Their Colonization into the Developing Mouse Embryos.Biotech (Basel (Switzerland)) · 2024Article
- Coupling during collective cell migration is controlled by a vinculin mechanochemical switch.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Vinculin is essential for sustaining normal levels of endogenous forces at cell-cell contacts.Biophysical journal · 2023Article
- Scribble, Lgl1, and myosin IIA interact with α-/β-catenin to maintain epithelial junction integrity.Cell adhesion & migration · 2023Article
- E-cadherin adhesion dynamics as revealed by an accelerated force ramp are dependent upon the presence of α-catenin.Biochemical and biophysical research communications · 2023Article
- Cingulin and paracingulin tether myosins-2 to junctions to mechanoregulate the plasma membrane.The Journal of cell biology · 2023Article
- Dual role of E-cadherin in cancer cells.Tissue barriers · 2022Review
- α-Catenin-dependent vinculin recruitment to adherens junctions is antagonistic to focal adhesions.Molecular biology of the cell · 2022Article
- Unique and redundant functions of cytoplasmic actins and nonmuscle myosin II isoforms at epithelial junctions.Annals of the New York Academy of Sciences · 2022Review
- Micron-scale supramolecular myosin arrays help mediate cytoskeletal assembly at mature adherens junctions.The Journal of cell biology · 2022Article
- Phenotypic Plasticity of Cancer Cells Based on Remodeling of the Actin Cytoskeleton and Adhesive Structures.International journal of molecular sciences · 2021Review
- Adherens junction regulates cryptic lamellipodia formation for epithelial cell migration.The Journal of cell biology · 2020Article
- Myosin II isoforms play distinct roles ineLife · 2019Article
- Keratin 6 regulates collective keratinocyte migration by altering cell-cell and cell-matrix adhesion.The Journal of cell biology · 2018Article
- Common and Specific Functions of Nonmuscle Myosin II Paralogs in Cells.Biochemistry. Biokhimiia · 2018Review
- The epithelial-mesenchymal transition induced by transcription factor LEF-1 is independent of β-catenin.Biochemistry and biophysics reports · 2018Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MDCK dog kidney epithelial cells express two isoforms of nonmuscle myosin heavy chain II, IIA and IIB. Using the CRISPR/Cas9 system, we established cells in which the IIA gene was ablated. These cells were then transfected with a vector that expresses GFP-IIA chimeric molecule under the control of a tetracycline-responsible element. In the absence of Dox (doxycyclin), when GFP-IIA is expressed (GFP-IIA+), the cells exhibit epithelial cell morphology, but in the presence of Dox, when expression of GFP-IIA is repressed (GFP-IIA-), the cells lose epithelial morphology and strong cell-cell adhesion. Consistent with these observations, GFP-IIA- cells failed to assemble junction components such as E-cadherin, desmoplakin, and occludin at cell-cell contact sites. Therefore, IIA is required for assembly of junction complexes. MDCK cells with an ablation of the α-catenin gene also exhibited the same phenotype. However, when in GFP-IIA- cells expressed α-catenin lacking the inhibitory region or E-cadherin/α-catenin chimeras, the cells acquired the ability to establish the junction complex. These experiments reveal that IIA acts as an activator of α-catenin in junction assembly.
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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.