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A more recent version of this article appeared on February 24, 2006
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M510004200v1
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Papers In Press, published online ahead of print December 22, 2005
J. Biol. Chem, 10.1074/jbc.M510004200
Submitted on September 12, 2005
Revised on December 20, 2005
Accepted on December 22, 2005

OAZ regulates BMP signaling through SMAD6 activation

Manching Ku, Shavonne Howard, Weihua Ni, Giorgio Lagna, and Akiko Hata

Molecular Cardiology Research Institute, Tufts-New England Medical Center, Boston, MA 02111

Corresponding Author: akiko.hata{at}tufts.edu

The intensity and duration of activation of a signal transduction system are important determinants of the specificity of the cellular response to the stimulus. It is unclear how different cells can generate a signal of varying intensity and duration in response to the same cytokine. We investigated the role of the transcriptional activator and Smad1/4 cofactor OAZ in regulating BMP signaling. We demonstrate that upon BMP4 stimulation, an OAZ-Smad1/4 complex binds to and activates the gene encoding Smad6, a specific inhibitor of the BMP pathway. Removal of endogenous OAZ from pluripotent embryonal carcinoma cells prevents the induction of Smad6 by BMP4 and extends the period of detection of phosphorylated Smad1 after BMP stimulation. Conversely, in cells that do not normally express OAZ, such as myoblasts and smooth muscle cells, forced OAZ expression leads to faster and higher Smad6 induction in response to BMP4, decrease of Smad1 phosphorylation and attenuation of BMP-mediated responses. Our results demonstrate that OAZ can alter the intensity and duration of the BMP stimulus through Smad6, and indicate that the tissue-specific expression of OAZ is a critical determinant of the cellular response to the BMP signal.


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