作者: Martha M. Monick , A. Brent Carter , Pamela K. Robeff , Dawn M. Flaherty , Michael W. Peterson
DOI: 10.4049/JIMMUNOL.166.7.4713
关键词:
摘要: Exposure of human alveolar macrophages to bacterial LPS results in activation a number signal transduction pathways. An early event after the macrophage comes contact with is phosphatidylinositol 3 kinase (PI 3-kinase). This study evaluates downstream effects that activation. We observed exposure phosphorylation Akt (serine 473). found this using both phosphorylation-specific Abs and also by vivo (32)P-loaded cells. AKT resulted phosphorylation-dependent inactivation glycogen synthase (GSK-3) 21/9). these events were linked PI 3-kinase because inhibitors, wortmannin LY294002, inhibited LPS-induced GSK-3. Inactivation GSK-3 has been shown reduce ubiquitination beta-catenin, resulting nuclear accumulation transcriptional activity beta-catenin. Consistent this, we caused an increase amounts 3-kinase-dependent beta-catenin expression genes require for their first demonstration activates AKT, inactivates GSK-3, causes nucleus any cell, including macrophages.