Association of HTLV Tax proteins with TAK1-binding protein 2 and RelA in calreticulin-containing cytoplasmic structures participates in Tax-mediated NF-κB activation

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• 作者：Francesca Avesani ; Maria Grazia Romanelli ; Marco Turci ; Gianfranco Di Gennaro ; Carla Sampaio ; Carlo Bidoia ; Umberto Bertazzoni ; Franç ; oise Bex
• 关键词：TAB2 ; RelA ; Tax ; NF-κ ; B ; HTLV ; Signalling ; Transactivation ; Calreticulin
• 刊名：Virology
• 出版年：2010
• 出版时间：5 December 2010
• 年：2010
• 卷：408
• 期：1
• 页码：39-48
• 全文大小：2370 K

文摘

HTLV-1 is more pathogenic than HTLV-2 despite having a similar genome and closely related transactivating oncoproteins. Both Tax-1 protein from HTLV-1 and Tax-2 from HTLV-2 activate the NF-κB pathway. The mechanisms involved in Tax-1 deregulation of this signalling pathway have been thoroughly investigated, but little is known about regulation by Tax-2. We have compared the interaction of Tax-1 and Tax-2 with two key NF-κB signalling factors: TAK1-binding protein 2 (TAB2), an adaptor involved in the activation of TAK1 kinase, and RelA, the active subunit of the canonical RelA/p50 NF-κB transcription factor. Tax-2 formed stable complexes with both RelA and TAB2. These two NF-κB factors colocalized with Tax proteins in dotted cytoplasmic structures targeted by calreticulin, a multi-process calcium-buffering chaperone. Co-expression of RelA and/or TAB2 markedly increased Tax-mediated NF-κB activation. These findings provide new insights into the role of RelA, TAB2 and Tax in the deregulation of the NF-κB pathway.