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Research Areas
adipocyte differentiation; cell proliferation; IGF-1 receptor signaling; caveolae; lipid rafts; centrosome; protein kinase B/Akt; cortactin; GLUT4; primary cilium; foam cell; macrophage; atherosclerosis; protein-lipid interaction; F-actin
Research Interests
Cell differentiation and proliferation are two reciprocally inhibited events. Growth arrest is the first step for 3T3-L1 adipocyte differentiation (1-3). Adipocyte differentiation can not be induced in proliferating 3T3-L1 cells. To induce adipocyte differentiation, growth arrested 3T3-L1 preadipocyte is induced by hormonal regimen (isobutylmethylxanthine, dexamethasone and insulin) (4-7). IGF-1 receptor signal is one of the most important induction signals (6-8). We are interested in how growth arrest prepares 3T3-L1 preadipocyte for differentiation induction and its effect on IGF-1 receptor signal transduction. We are also interested in the function of membrane lipid microdomains in IGF-1 receptor transmembrane signaling.
Protein tyrosine phosphorylation and mitotic regulation are often related to each other. The identification of tyrosine phosphorylated cortactin in regulation of centrosome separation has prompted us to further explore the function of cortactin and its phosphorylation. As an anchor for F-actin, tyrosine phosphorylated cortactin provides a regulation of F-actin attachment by phosphorylation turnover. By regulating cortactin tyrosine phosphorylation, F-actin driven cellular movement can be directed and controlled (9). We are especially interested in the proteins interacted with tyrosine phosphorylated form of cortactin and their functions in microfilament system.
adipocyte differentiation; cell proliferation; IGF-1 receptor signaling; caveolae; lipid rafts; centrosome; protein kinase B/Akt; cortactin; GLUT4; primary cilium; foam cell; macrophage; atherosclerosis; protein-lipid interaction; F-actin
Research Interests
Cell differentiation and proliferation are two reciprocally inhibited events. Growth arrest is the first step for 3T3-L1 adipocyte differentiation (1-3). Adipocyte differentiation can not be induced in proliferating 3T3-L1 cells. To induce adipocyte differentiation, growth arrested 3T3-L1 preadipocyte is induced by hormonal regimen (isobutylmethylxanthine, dexamethasone and insulin) (4-7). IGF-1 receptor signal is one of the most important induction signals (6-8). We are interested in how growth arrest prepares 3T3-L1 preadipocyte for differentiation induction and its effect on IGF-1 receptor signal transduction. We are also interested in the function of membrane lipid microdomains in IGF-1 receptor transmembrane signaling.
Protein tyrosine phosphorylation and mitotic regulation are often related to each other. The identification of tyrosine phosphorylated cortactin in regulation of centrosome separation has prompted us to further explore the function of cortactin and its phosphorylation. As an anchor for F-actin, tyrosine phosphorylated cortactin provides a regulation of F-actin attachment by phosphorylation turnover. By regulating cortactin tyrosine phosphorylation, F-actin driven cellular movement can be directed and controlled (9). We are especially interested in the proteins interacted with tyrosine phosphorylated form of cortactin and their functions in microfilament system.
Research Interests
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