ATBF1 enhances the suppression of STAT3 signaling by interaction with PIAS3

被引:54
作者
Nojiri, S
Joh, T
Miura, Y
Sakata, N
Nomura, T
Nakao, H
Sobue, S
Oharra, H
Asai, K
Ito, M
机构
[1] Nagoya City Univ, Grad Sch Med Sci, Dept Mol Neurobiol, Mizuho Ku, Nagoya, Aichi 4678601, Japan
[2] Nagoya City Univ, Grad Sch Med Sci, Dept Internal Med & Bioregulat, Mizuho Ku, Nagoya, Aichi 4678601, Japan
[3] Showa Pharmaceut Univ, Dept Biochem, Machida, Tokyo 1948543, Japan
关键词
D O I
10.1016/j.bbrc.2003.12.054
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
ATBF1 was first discovered as a suppressor of AFP expression in hepatocytes. It is present in brain, adult liver, lung, and gastrointestinal 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. (C) 2003 Elsevier Inc. All rights reserved.
引用
收藏
页码:97 / 103
页数:7
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