Phosphatidylinositol 3-Kinase/Akt Pathway Targets Acetylation of Smad3 through Smad3/CREB-binding Protein Interaction
Copyright policy )Phosphatidylinositol 3-Kinase/Akt Pathway Targets Acetylation of Smad3 through Smad3/CREB-binding Protein Interaction
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.
- Johns Hopkins University United States
- Paris 13 University France
- Johns Hopkins Medicine United States
- University of Paris France
- Hospital Paul Brousse France
Gene Expression Regulation, Viral, Mitogen-Activated Protein Kinase 1, Herpesvirus 4, Human, Mitogen-Activated Protein Kinase 3, MAP Kinase Signaling System, Acetylation, lymphomas, CREB-Binding Protein, Transforming Growth Factor beta1, Phosphatidylinositol 3-Kinases, Viral Proteins, Salud pública, Cell Line, Tumor, Trans-Activators, Humans, Virus Activation, Smad3 Protein, Proto-Oncogene Proteins c-akt
Gene Expression Regulation, Viral, Mitogen-Activated Protein Kinase 1, Herpesvirus 4, Human, Mitogen-Activated Protein Kinase 3, MAP Kinase Signaling System, Acetylation, lymphomas, CREB-Binding Protein, Transforming Growth Factor beta1, Phosphatidylinositol 3-Kinases, Viral Proteins, Salud pública, Cell Line, Tumor, Trans-Activators, Humans, Virus Activation, Smad3 Protein, Proto-Oncogene Proteins c-akt
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