ATBF1 enhances the suppression of STAT3 signaling by interaction with PIAS3
ATBF1 enhances the suppression of STAT3 signaling by interaction with PIAS3
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DOI：
10.1016/j.bbrc.2003.12.054
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发表时间：
2004-01-30
影响因子：
3.1
通讯作者：
Ito, M
中科院分区：
文献类型：
--
作者：
Nojiri, S;Joh, T;Ito, M
ATBF 1首先被发现是肝细胞中AFP表达的抑制因子。存在于脑、成人肝、肺和胃肠道中。最近，有报道ATBF 1调节成肌细胞分化，并与v-Myb相互作用调节其反式激活。使用酵母双杂交系统，我们寻找蛋白质蛋白质相互作用，以发现ATBF 1的新功能。我们在这里提出的实验证据表明，ATBF 1是一个新的调节因子STAT 3介导的信号转导，通过其与PIAS 3的相互作用。PIAS 3因此被鉴定为ATBF 1结合蛋白。在共转染实验中，发现全长ATBF 1在Hep G2细胞中与PIAS 3形成复合物。在荧光素酶测定中，发现ATBF 1对IL-6刺激诱导的STAT 3信号传导没有影响，但它确实协同增强PIAS 3对活化的STAT 3的抑制。总之，ATBF 1可通过与PIAS 3共同作用抑制IL-6介导的细胞应答。(C)2003年爱思唯尔公司All rights reserved.
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.