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The early region 1A 52R polypeptide, a protein expressed
exclusively by the in vivo oncogenic adenovirus subtype 12,
represses the trans-activating function of the cellular
transcription factor complex AP-1 consisting of c-Jun-c-Jun homodimers.
In this report we demonstrate that the repression in vivo correlates with a direct physical interaction of the adenovirus
protein with c-Jun in vitro. Interestingly, the 52R protein
binds to the bZIP domain of c-Jun essential for dimerization and DNA
binding but not to the c-Jun activation domain. This interaction does
not prevent the promoter binding of c-Jun/AP-1. Moreover, the physical
association between c-Jun and the TATA box-binding protein TBP is not
disturbed by the 52R polypeptide. In fact, we show evidence that
down-regulation of c-Jun activity by the adenoviral protein is due to
the inhibition of phosphorylation of the c-Jun
trans-activation domain. In vivo phosphorylation of
the c-Jun activation domain is necessary for the interaction of c-Jun
with specific cofactors such as CBP and therefore a prerequisite for
the activation of target genes. Due to these results we propose a model
in which the 52R protein represses the trans-activating
function of c-Jun by preventing its phosphorylation through a specific
kinase necessary for the activation of the cellular transcription
factor.
Volume 270,
Number 18,
Issue of May 5, pp. 10754-10763, 1995
©1995 by The American Society for Biochemistry and Molecular Biology, Inc.
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