Jin D Y, Giordano V, Kibler K V, Nakano H, Jeang K T
Laboratory of Molecular Microbiology, NIAID, National Institutes of Health, Bethesda, Maryland 20892-0460, USA.
J Biol Chem. 1999 Jun 18;274(25):17402-5. doi: 10.1074/jbc.274.25.17402.
Mechanisms by which the human T-cell leukemia virus type I Tax oncoprotein activates NF-kappaB remain incompletely understood. Although others have described an interaction between Tax and a holo-IkappaB kinase (IKK) complex, the exact details of protein-protein contact are not fully defined. Here we show that Tax binds to neither IKK-alpha nor IKK-beta but instead complexes directly with IKK-gamma, a newly characterized component of the IKK complex. This direct interaction with IKK-gamma correlates with Tax-induced IkappaB-alpha phosphorylation and NF-kappaB activation. Thus, our findings establish IKK-gamma as a key molecule for adapting an oncoprotein-specific signaling to IKK-alpha and IKK-beta.
人T细胞白血病病毒I型(HTLV-I)Tax癌蛋白激活核因子-κB(NF-κB)的机制仍未完全明确。尽管其他人已描述了Tax与全酶IκB激酶(IKK)复合物之间的相互作用,但蛋白质-蛋白质接触的确切细节尚未完全确定。在此我们表明,Tax既不与IKK-α结合,也不与IKK-β结合,而是直接与IKK-γ形成复合物,IKK-γ是IKK复合物新鉴定的一个组分。这种与IKK-γ的直接相互作用与Tax诱导的IκB-α磷酸化及NF-κB激活相关。因此,我们的研究结果确立了IKK-γ作为使癌蛋白特异性信号转导适配于IKK-α和IKK-β的关键分子。