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J. Biol. Chem., Vol. 276, Issue 30, 27944-27949, July 27, 2001

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Induction of AP-2 Expression by Adenoviral Infection Involves Inactivation of the AP-2rep Transcriptional Corepressor CtBP1^*

Marion Schuierer, Kristina Hilger-Eversheim^§, Thomas Dobner, Anja-Katrin Bosserhoff^§, Markus Moser^§, Jeremy Turner^¶, Merlin Crossley^¶, and Reinhard Buettner^§

From the  Institute for Microbiology, University of Regensburg Medical School, Franz-Josef-Strauss-Allee 11, D-93042 Regensburg, Germany, the ^§ Institute of Pathology, University Hospital RWTH Aachen, Pauwelsstrasse 30, D-52074 Aachen, Germany, and the ^¶ Department of Biochemistry, G08, University of Sydney, Sydney, New South Wales 2006, Australia

AP-2 transcription factors execute important functions during embryonic development and malignant transformation. Recently, we have isolated a transcriptional repressor of AP-2 expression, the novel Krüppel-related zinc finger protein AP-2rep (Klf12). Here, we show that repression of AP-2 transcription by AP-2rep is dependent on an N-terminal PVDLS motif that interacts specifically with the corepressor CtBP1 both in vivo and in vitro. This interaction motif was previously identified in the C-terminal region of the adenoviral oncoprotein E1A. Infection of both HeLa and PA-1 cells with adenovirus type 5 strongly induced AP-2 mRNA. Consistently, E1A was necessary and sufficient to mediate up-regulation of AP-2. Transiently transfected wild-type E1A protein activated an AP-2rep sensitive cis-regulatory element of the AP-2 promoter, but E1A protein harboring a mutation in the PVDLS motif failed to activate. In summary, we conclude that the adenoviral oncoprotein E1A activates transcription from the endogenous AP-2 gene, an effect that involves transcriptional derepression of the AP-2 promoter by interaction of E1A with the AP-2rep corepressor CtBP1.

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