| Autor: |
Ponce DP; Institute of Biomedical Sciences, Cell Transformation Laboratory, Program of Cellular and Molecular Biology, ICBM, University of Chile, Av. Independencia 1027, 8700664 Santiago, Chile., Yefi R, Cabello P, Maturana JL, Niechi I, Silva E, Galindo M, Antonelli M, Marcelain K, Armisen R, Tapia JC |
| Jazyk: |
angličtina |
| Zdroj: |
Molecular and cellular biochemistry [Mol Cell Biochem] 2011 Oct; Vol. 356 (1-2), pp. 127-32. Date of Electronic Publication: 2011 Jul 07. |
| DOI: |
10.1007/s11010-011-0965-4 |
| Abstrakt: |
β-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 β-catenin transcriptional activity, whereas CK2 hyperactivates AKT by phosphorylation at Ser129; however, the role of this phosphorylation on β-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 β-catenin subcellular localization and transcriptional activity and survivin expression. CK2α overexpression led to an augmented β-catenin-dependent transcription and protein levels of survivin, and consequently an enhanced resistance to apoptosis. However, CK2α-enhancing effects were reversed when an AKT mutant deficient in Ser129 phosphorylation by CK2 was co-expressed. Therefore, our results strongly suggest that CK2α-specific enhancement of β-catenin transcriptional activity as well as cell survival may depend on AKT hyperactivation by CK2. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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