Is there a role for ubiquitin or SUMO in human T-cell leukemia virus type 2 Tax-induced NF-κB activation?
Is there a role for ubiquitin or SUMO in human T-cell leukemia virus type 2 Tax-induced NF-κB activation?
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DOI：
10.2217/fvl.13.1
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发表时间：
2013-03
期刊：
影响因子：
3.1
通讯作者：
Harhaj EW
中科院分区：
文献类型：
--
作者：
Lavorgna A;Harhaj EW
已经确定，人类T细胞白血病病毒1型编码的癌蛋白Tax（Tax 1）经历多聚泛素化作为其持续激活NF-κB机制的一部分。然而，目前仍不清楚Tax 2编码的密切相关的人类T细胞白血病病毒2型利用任何翻译后机制，以激活NF-κB。本研究探讨泛素化和SUMO化在Tax 2活化NF-κB中的作用。作者已经证明，与Tax 1相反，Tax 2不与泛素或SUMO蛋白缀合。E2泛素结合酶Ubc 13的过表达特异性地增强Tax 1，而不是Tax 2，泛素化和NF-κB活化。此外，不能被泛素化、SUMO化或乙酰化的Tax 2无赖氨酸突变体保留了NEMO/IKKγ相互作用和NF-κB途径的激活。总之，这些结果提供了Tax 1和Tax 2利用不同机制激活NF-κB的证据。
It is well established that the human T-cell leukemia virus type 1-encoded oncoprotein Tax (Tax1) undergoes polyubiquitination as part of its mechanism to persistently activate NF-κB. However, it remains unclear whether Tax2 encoded by the closely related human T-cell leukemia virus type 2 utilizes any post-translational mechanisms to activate NF-κB. This study examines the role of ubiquitination and SUMOylation in Tax2 activation of NF-κB. The authors have demonstrated that, in contrast to Tax1, Tax2 is not conjugated by ubiquitin or SUMO proteins. Overexpression of the E2 ubiquitin-conjugating enzyme Ubc13 specifically enhances Tax1, but not Tax2, ubiquitination and NF-κB activation. Furthermore, a Tax2 lysineless mutant that is unable to be ubiquitinated, SUMOylated or acetylated retains NEMO/IKKγ interactions and activation of the NF-κB pathway. Together, these results provide evidence that Tax1 and Tax2 utilize distinct mechanisms to activate NF-κB.
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