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c-Cbl functions as a multifunctional adaptor and an E3 ubiquitin protein ligase. Several studies have shown that c-Cbl is involved in cytoskeleton-mediated events , but the molecular mechanisms linking c-Cbl to cytoskeletal rearrangements remain to be elucidated. To understand the role of c-Cbl in regulation of cytoskeleton-dependent cellular functions, we assessed the roles of endogenous Rac1, RhoA and Rap1 in the c-Cbl-dependent spreading and migration of v-Abl-transformed fibroblasts overexpressing c-Cbl, using RNAi. Glioma invasion is involved in multiple biological processes which are…mehr

Produktbeschreibung
c-Cbl functions as a multifunctional adaptor and an E3 ubiquitin protein ligase. Several studies have shown that c-Cbl is involved in cytoskeleton-mediated events , but the molecular mechanisms linking c-Cbl to cytoskeletal rearrangements remain to be elucidated. To understand the role of c-Cbl in regulation of cytoskeleton-dependent cellular functions, we assessed the roles of endogenous Rac1, RhoA and Rap1 in the c-Cbl-dependent spreading and migration of v-Abl-transformed fibroblasts overexpressing c-Cbl, using RNAi. Glioma invasion is involved in multiple biological processes which are primarily associated with cytoskeleton-mediated events including adhesion, migration, and degradation of extra cellular matrix (ECM). In this study, we examined biological roles of c-Cbl using RNAi-mediated depletion of endogenous c-Cbl and stably c-Cbl expressing glioma cells generated by lentiviral transduction and showed that c-Cbl increases invasion through degradation of ECM by upregulation of MMP2 but not through migration, adhesion, or growth of SNB19 glioblastoma cell line.
Autorenporträt
Dr. Hojin Lee is currently working as an Associate Research Scientist in the Department of Pharmacology at Yale University School of Medicine.He received Ph.D. at Temple University school of Medicine and B.S. at Korea University. His research has been focused on understanding cellular signal transduction pathways in health and disease.