title: v-Crk regulates membrane dynamics and Rac activation.
abstract: Cell migration is an integrated process that involves cell adhesion, protrusion and contraction. We recently used CAS (Crk-associated substrate, 130CAS)-deficient mouse embryo fibroblasts (MEFs) to examined contribution made to v-Crk to that process via its interaction with Rac1. v-Crk, the oncogene product of avian sarcoma virus CT10, directly affects membrane ruffle formation and is associated with Rac1 activation, even in the absence of CAS, a major substrate for Crk. In CAS-deficient MEFs, cell spreading and lamellipodium dynamics are delayed; moreover, Rac activation is significantly reduced and it is no longer targeted to the membrane. However, expression of v-Crk by CAS-deficient MEFs increased cell spreading and active lamellipodium protrusion and retraction. v-Crk expression appears to induce Rac1 activation and its targeting to the membrane, which directly affects membrane dynamics and, in turn, cell migration. It thus appears that v-Crk/Rac1 signaling contributes to the regulation of membrane dynamics and cell migration, and that v-Crk is an effector molecule for Rac1 activation that regulates cell motility.
authors.affiliation: Cell Dynamics Research Center and Bioimaging Research Center, Department of Life Science, Gwangju Institute of Science and Technology, Buk-gu, Gwangju, Korea.
authors.forename: Myeong Gu
authors.initials: MG
authors.lastname: Yeo
authors.forename: Woo Keun
authors.initials: WK
authors.lastname: Song
mesh_terms: D000818:Animals; D002462:Cell Membrane / Q000378:metabolism*; D004789:Enzyme Activation; D050736:Oncogene Protein v-crk / Q000378:metabolism*; D015398:Signal Transduction; D020744:rac GTP-Binding Proteins / Q000378:metabolism*
chemical_list: D050736:Oncogene Protein v-crk; D020744:rac GTP-Binding Proteins