| Autor: |
Ponce, Daniela, Yefi, Roger, Cabello, Pablo, Maturana, Jose, Niechi, Ignacio, Silva, Eduardo, Galindo, Mario, Antonelli, Marcelo, Marcelain, Katherine, Armisen, Ricardo, Tapia, Julio |
| Zdroj: |
Molecular & Cellular Biochemistry; Oct2011, Vol. 356 Issue 1/2, p127-132, 6p |
| 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. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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