HTLV-1 tax-mediated TAK1 activation involves TAB2 adapter protein
HTLV-1 tax-mediated TAK1 activation involves TAB2 adapter protein
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DOI：
10.1016/j.bbrc.2007.10.172
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发表时间：
2008-01-04
影响因子：
3.1
通讯作者：
Takaesu, Giichi
中科院分区：
文献类型：
--
作者：
Yu, Qingsheng;Minoda, Yasumasa;Takaesu, Giichi
人T细胞白血病病毒I型（HTLV-1）Tax是一种癌蛋白，在HTLV-1感染的T淋巴细胞的增殖和转化中起关键作用。最近有报道称，Tax激活了MAPKKK家族TAK 1。然而，Tax介导的TAK 1激活的分子机制还不清楚。在这份报告中，我们研究了TAK 1结合蛋白2（TAB 2）在Tax介导的TAK 1激活中的作用。我们发现TAB 2与Tax发生物理相互作用，并增强Tax诱导的NF-κ B活性。Tax和TAB 2在共表达时协同激活TAK 1。此外，TAK 1被Tax激活需要TAB 2结合以及Tax的泛素化。我们还发现TRAF 2、5或6的过表达强烈诱导Tax泛素化。这些结果表明，TAB 2可能是至关重要的参与Tax介导的TAK 1的激活和NF-κ B激活TRAF家族蛋白是潜在的细胞E3泛素连接酶对Tax。(c)2007爱思唯尔公司All rights reserved.
Human T cell leukemia virus type I (HTLV-1) Tax is an oncoprotein that plays a crucial role in the proliferation and transformation of HTLV-1-infected T lymphocytes. It has recently been reported that Tax activates a MAPKKK family, TAK1. However, the molecular mechanism of Tax-mediated TAK1 activation is not well understood. In this report, we investigated the role of TAK1-binding protein 2 (TAB2) in Tax-mediated TAK1 activation. We found that TAB2 physically interacts with Tax and augments Tax-induced NF-kappa B activity. Tax and TAB2 cooperatively activate TAK1 when they are coexpressed. Furthermore, TAK1 activation by Tax requires TAB2 binding as well as ubiquitination of Tax. We also found that the overexpression of TRAF2, 5, or 6 strongly induces Tax ubiquitination. These results suggest that TAB2 may be critically involved in Tax-mediated activation of TAK1 and that NF-kappa B-activating TRAF family proteins are potential cellular E3 ubiquitin ligases toward Tax. (c) 2007 Elsevier Inc. All rights reserved.