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Title

AKT2 interacts with Snail1 in the E-cadherin Promoter

AuthorsVillagrasa, P.; Diaz, V.M.; Viñas-Castells, R.; Peiro, S.; Valle-Perez, Beatriz del; Dave, N.; Rodriguez-Asiain, A.; Casal, J. Ignacio ; Lizcano, J. M.; Duñach, Mireia; García de Herreros, Antonio
KeywordsSnail1
EMT
Akt
E-cadherin
Issue Date12-Dec-2011
PublisherNature Publishing Group
CitationOncogene
AbstractSnail1 is a transcriptional factor essential for triggering epithelial-to-mesenchymal transition. Moreover, Snail1 promotes resistance to apoptosis, an effect associated to PTEN gene repression and Akt stimulation. In this article we demonstrate that Snail1 activates Akt at an additional level, as it directly binds to and activates this protein kinase. The interaction is observed in the nucleus and increases the intrinsic Akt activity. We determined that Akt2 is the isoform interacting with Snail1, an association that requires the pleckstrin homology domain in Akt2 and the C-terminal half in Snail1. Snail1 enhances the binding of Akt2 to the E-cadherin (CDH1) promoter and Akt2 interference prevents Snail1 repression of CDH1 gene. We also show that Snail1 binding increases Akt2 intrinsic activity on histone H3 and have identified Thr45 as a residue modified on this protein. Phosphorylation of Thr45 in histone H3 is sensitive to Snail1 and Akt2 cellular levels; moreover, Snail1 upregulates the binding of phosphoThr45 histone H3 to the CDH1 promoter. These results uncover an unexpected role of Akt2 in transcriptional control and point out to phosphorylation of Thr45 in histone H3 as a new epigenetic mark related to Snail1 and Akt2 action.Oncogene advance online publication
Description7 figuras
Publisher version (URL)http://dx.doi.org/ 10.1038/onc.2011.562
URIhttp://hdl.handle.net/10261/50517
DOI10.1038/onc.2011.562
ISSN0950-9232
E-ISSN1476-5594
Appears in Collections:(CIB) Artículos
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