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Papers In Press, published online ahead of print May 23, 2001
J. Biol. Chem, 10.1074/jbc.M100070200
Submitted on January 4, 2001
Revised on May 21, 2001
Accepted on May 22, 2001
Institute of Pathology, University Hospital RWTH Aachen, D-52074 Aachen D-52074
Corresponding Author: Buettner{at}pat.rwth-aachen.de
AP-2 transcription factors execute important functions during embryonic development and malignant transformation. Recently, we have isolated a transcriptional repressor of AP-2a expression, the novel Krüppel-related zinc finger protein AP-2rep (Klf12). Here we show that repression of AP-2a 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-2a mRNA. Consistently, E1A was necessary and sufficient to mediate upregulation of AP-2a. Transiently transfected wild-type E1A protein activated an AP-2rep sensitive cis-regulatory element of the AP-2a 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-2a gene, an effect that involves transcriptional derepression of the AP-2a promoter by interaction of E1A with the AP-2rep corepressor CtBP1.
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