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

作者：Avesani Francesca; Romanelli Maria Grazia; Turci Marco; Di Gennaro Gianfranco; Sampaio Carla; Bidoia Carlo; Bertazzoni Umberto^*; Bex Francoise

来源：Virology, 2010, 408(1): 39-48.

DOI：10.1016/j.virol.2010.08.023

• TAB2
• RelA
• Tax
• NF-kappa B
• HTLV
• Signalling
• Transactivation
• Calreticulin

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-kappa B 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-kappa B 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-kappa B transcription factor. Tax-2 formed stable complexes with both RelA and TAB2. These two NF-kappa B 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-kappa B activation. These findings provide new insights into the role of RelA, TAB2 and Tax in the deregulation of the NF-kappa B pathway.

• 出版日期2010-12-5