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M404428200v1
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Papers In Press, published online ahead of print May 15, 2004
J. Biol. Chem, 10.1074/jbc.M404428200
Submitted on April 21, 2004
Revised on May 15, 2004
Accepted on May 14, 2004

The transcriptional Co-activator p/CIP (NCoA-3) is upregulated by STAT6 and serves as a positive regulator of transcriptional activation by STAT6

Akinori Arimura, Maartje van Peer, Andreas J. Schroeder, and Paul Rothman

Medicine and Microbilogy, Columbia University, New York, NY 10032

Corresponding Author: pbr3{at}columbia.edu

Transcriptional activation by signal transducer and activator of transcription 6 (STAT6) has been shown to require the direct interaction not only with coactivators such as p300, CREB-binding protein (CBP) but also with nuclear coactivator 1 (NCoA-1), a member of the p160/steroid receptor coactivator family. Among the p160/steroid receptor coactivators, only p/CIP (NCoA-3) has been shown to be up-regulated by IL-4 in B cells through a STAT-6-dependent mechanism using GeneChip analysis. In this study, we have investigated the function of p/CIP in the transcriptional activation by STAT6. We found that p/CIP indirectly interacted with STAT6 via p300 and overexpression of CBP interacting domain of p/CIP (p/CIP947-1084) prevented the interaction of p/CIP with STAT6 by blocking the binding of p/CIP to p300. Whereas expression of p/CIP947-1084 resulted in a marked reduction of STAT6-mediated transactivation, overexpression of wild type p/CIP resulted in significant enhancement of it. In addition, p/CIP947-1084 markedly reduced CD23 expression on B cells stimulated with IL-4 whereas overexpression of wild type p/CIP enhanced it. Chromatin immuoprecipitations demonstrate that IL-4 increases the interaction of p/CIP with the murine immunoglobulin heavy-chain germ line epsilon promoter in B cells. These results suggest that p/CIP positively regulates STAT6 transcriptional activation through formation of a STAT6, p300/CBP and p/CIP complex.


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