Sensing of Cytoskeletal Forces by Asymmetric Adherens Junctions
Autor: | Tsveta S. Malinova, Stephan Huveneers |
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Přispěvatelé: | Graduate School, Medical Biochemistry, ACS - Amsterdam Cardiovascular Sciences, AGEM - Amsterdam Gastroenterology Endocrinology Metabolism, ACS - Diabetes & metabolism, ACS - Microcirculation, ACS - Atherosclerosis & ischemic syndromes |
Jazyk: | angličtina |
Rok vydání: | 2018 |
Předmět: |
0301 basic medicine
Biology Mechanotransduction Cellular Models Biological Adherens junction 03 medical and health sciences 0302 clinical medicine Cell–cell interaction Animals Humans BAR domain Mechanotransduction Cytoskeleton Cadherin Cell Membrane Actomyosin Adherens Junctions Cell Biology Cadherins Endocytosis Cell biology 030104 developmental biology Membrane curvature Amphiphysin 030217 neurology & neurosurgery |
Zdroj: | Trends in cell biology, 28(4), 328-341. Elsevier Limited |
ISSN: | 0962-8924 |
Popis: | Within tissues, key cellular adaptations occur via mechanotransduction responses at cell-cell junctions. Adherens junctions (AJs) typically form between cells as a result of the binding of cadherin receptors of the same type (homotypic), and are linked to the force-propagating and -generating actomyosin cytoskeleton. Recent studies have found that AJs maintain monolayer integrity in dynamic tissues and drive collective cell behavior by converting into asymmetric remodeling entities. Here, we overview the molecular processes that may explain how asymmetric cell-cell junctions sense differences in cytoskeletal geometry between cells. We discuss the link between cadherin-complex dynamics and the actomyosin cytoskeleton at asymmetric cell-cell junctions. We then outline the role of Bin/Amphiphysin/Rvs (BAR) proteins, cytoplasmic regulators of endocytosis and cytoskeletal dynamics that sense force-induced membrane curvature, at AJs undergoing asymmetric remodeling. Lastly, we highlight the physiological importance of junctional asymmetry for epithelial and vascular tissue and discuss its potential role in disease. |
Databáze: | OpenAIRE |
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