Phosphatidylinositol 3-kinase/Akt pathway targets acetylation of Smad3 through Smad3/CREB-binding protein interaction: contribution to transforming growth factor beta1-induced Epstein-Barr virus reactivation.

Epstein-Barr virus, a ubiquitous human herpesvirus, is associated with the development of carcinomas and lymphomas. We previously showed that transforming growth factor beta1 (TGF-beta1) mediated the virus to enter the lytic cycle, which is triggered by expression of Z Epstein-Barr virus replication activator (ZEBRA), through the ERK 1/2 MAPK signaling ...
pathway. We report here that Akt, activated downstream from ERK 1/2, was required for TGF-beta1-induced ZEBRA expression and enabled Smad3, a mediator of TGF-beta1 signaling, to be acetylated by direct interaction with the co-activator CREB-binding protein and then to regulate TGF-beta1-induced ZEBRA expression.
Mesh Terms:
Acetylation, CREB-Binding Protein, Cell Line, Tumor, Gene Expression Regulation, Viral, Herpesvirus 4, Human, Humans, MAP Kinase Signaling System, Mitogen-Activated Protein Kinase 1, Mitogen-Activated Protein Kinase 3, Phosphatidylinositol 3-Kinases, Proto-Oncogene Proteins c-akt, Smad3 Protein, Trans-Activators, Transforming Growth Factor beta1, Viral Proteins, Virus Activation
J. Biol. Chem.
Date: Sep. 04, 2009
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