期刊
MOLECULAR AND CELLULAR BIOCHEMISTRY
卷 356, 期 1-2, 页码 127-132出版社
SPRINGER
DOI: 10.1007/s11010-011-0965-4
关键词
CK2; AKT/PKB; beta-Catenin; Survivin; Cancer
类别
beta-Catenin is crucial in the canonical Wnt signaling pathway. This pathway is up-regulated by CK2 which is associated with an enhanced expression of the antiapoptotic protein survivin, although the underlying molecular mechanism is unknown. AKT/PKB kinase phosphorylates and promotes beta-catenin transcriptional activity, whereas CK2 hyperactivates AKT by phosphorylation at Ser129; however, the role of this phosphorylation on beta-catenin transcriptional activity and cell survival is unclear. We studied in HEK-293T cells, the effect of CK2-dependent hyperactivation of AKT on cell viability, as well as analyzed beta-catenin subcellular localization and transcriptional activity and survivin expression. CK2 alpha overexpression led to an augmented beta-catenin-dependent transcription and protein levels of survivin, and consequently an enhanced resistance to apoptosis. However, CK2 alpha-enhancing effects were reversed when an AKT mutant deficient in Ser129 phosphorylation by CK2 was co-expressed. Therefore, our results strongly suggest that CK2 alpha-specific enhancement of beta-catenin transcriptional activity as well as cell survival may depend on AKT hyperactivation by CK2.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据