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Inhibition of AP-1 by the glucocorticoid-inducible protein GILZ 总被引:27,自引:0,他引:27
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Janowski E Jiao X Katiyar S Lisanti MP Liu M Pestell RG Morad M 《The international journal of biochemistry & cell biology》2011,43(8):1104-1113
Tumor progression involves the acquisition of invasiveness through a basement membrane. The c-jun proto-oncogene is overexpressed in human tumors and has been identified at the leading edge of human breast tumors. TGF-β plays a bifunctional role in tumorigenesis and cellular migration. Although c-Jun and the activator protein 1 (AP-1) complex have been implicated in human cancer, the molecular mechanisms governing cellular migration via c-Jun and the role of c-Jun in TGF-β signaling remains poorly understood. Here, we analyze TGF-β mediated cellular migration in mouse embryo fibroblasts using floxed c-jun transgenic mice. We compared the c-jun wild type with the c-jun knockout cells through the use of Cre recombinase. Herein, TGF-β stimulated cellular migration and intracellular calcium release requiring endogenous c-Jun. TGF-β mediated Ca(2+) release was independent of extracellular calcium and was suppressed by both U73122 and neomycin, pharmacological inhibitors of the breakdown of PIP(2) into IP(3). Unlike TGF-β-mediated Ca(2+) release, which was c-Jun dependent, ATP mediated Ca(2+) release was c-Jun independent. These studies identify a novel pathway by which TGF-β regulates cellular migration and Ca(2+) release via endogenous c-Jun. 相似文献
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F L Day L A Rafty C N Chesterman L M Khachigian 《The Journal of biological chemistry》1999,274(34):23726-23733
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Freyssenet D Irrcher I Connor MK Di Carlo M Hood DA 《American journal of physiology. Cell physiology》2004,286(5):C1053-C1061
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