title: [p130Cas-Mediated Regulation of Mechanical Functions of Cells.]
abstract: It is 10 years since we reported Cas as a cell mechano-sensor that converts stretching force to a biochemical signal. While we have been looking into the mechanism of how Cas molecules are extended, it appears that the source of stretching force does not derive from actomyosin contraction, but originates from actin polymerization. Furthermore, we have found that phosphorylated Cas links actomyosin contraction to cell migration by tensin 1-mediated association with inwardly moving actin filaments. Collectively, Cas serves as a force sensor at the cell leading edges as well as a part of force transmission machinery, i.e. clutch, which drives the cell forward.
authors.affiliation: Department of Rehabilitation for the Movement Functions, Research Institute,National Rehabilitation Center for Persons with Disabilities, Japan.
authors.forename: Yasuhiro
authors.initials: Y
authors.lastname: Sawada
authors.affiliation: Mechanobiology Laboratory, Nagoya University Graduate School of Medicine, Japan.
authors.forename: Hiroaki
authors.initials: H
authors.lastname: Hirata
mesh_terms: D000199:Actins / Q000378:metabolism; D000818:Animals; D002448:Cell Adhesion; D050719:Crk-Associated Substrate Protein / Q000378:metabolism*; D006801:Humans; D040542:Mechanotransduction, Cellular; D010766:Phosphorylation
chemical_list: D000199:Actins; D050719:Crk-Associated Substrate Protein