par Avesani, Francesca;Romanelli, Maria Grazia;Turci, Marco;Di Gennaro, Gianfranco;Bidoia, Carlo;Bertazzoni, Umberto;Sampaio, Carla ;Bex, Françoise
Référence Virology, 408, 1, page (39-48)
Publication Publié, 2010-12
Référence Virology, 408, 1, page (39-48)
Publication Publié, 2010-12
Article révisé par les pairs
Résumé : | 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. © 2010 Elsevier Inc. |