Biochem Biophys Res Commun. 2004 Jan 30;314(1):97-103.

ATBF1 enhances the suppression of STAT3 signaling by interaction with PIAS3.

Nojiri S, Joh T, Miura Y, Sakata N, Nomura T, Nakao H, Sobue S, Ohara H, Asai K, Ito M.

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Department of Internal Medicine and Bioregulation, Nagoya City University Graduate School of Medical Sciences 1 Kawasumi, Mizuho-cho, Mizuho-ku, Nagoya, Japan.

Abstract

ATBF1 was first discovered as a suppressor of AFP expression in hepatocytes. It is present in brain, adult liver, lung, and gastro-intestinal tract. Recently, it has been reported that ATBF1 regulates myoblastic differentiation and interacts with v-Myb in regulation of its transactivation. Using the yeast two-hybrid system, we searched for protein-protein interactions to uncover new functions for ATBF1. We present here experimental evidence that ATBF1 is a new regulatory factor for STAT3-mediated signal transduction through its interaction with PIAS3. PIAS3 was thus identified as an ATBF1-binding protein. In co-transfection experiments, the full-length ATBF1 was found to form complexes with PIAS3 in Hep G2 cells. In the luciferase assay, ATBF1 was found to have no influence on STAT3 signaling induced by IL-6 stimulation, but it did synergistically enhance PIAS3 inhibition of activated STAT3. In conclusion, ATBF1 can suppress the IL-6-mediated cellular response by acting together with PIAS3.

PMID:: 14715251; [PubMed - indexed for MEDLINE]

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ATBF1 enhances the suppression of STAT3 signaling by interaction with PIAS3.
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Biochem Biophys Res Commun. 2004 Jan 30 ;314(1):97-103.

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