Abstract
Activation of the NF-κB transcription factors by the viral protein Tax plays a vital role in the pathogenesis of diseases associated with human T-cell lymphotropic virus type I (HTLV-I). The Tax oncoprotein undergoes constitutive K63-linked ubiquitination and sumoylation; however, the roles and molecular mechanisms of these post-translational modifications in Tax-mediated NF-κB activation are being debated. Here, we discuss our current understanding of Tax activation of NF-κB, with a focus on the controversies and the challenges that we are facing.
Highlights
Human T-cell lymphotropic virus type I (HTLV-I) is the etiological agent of adult T-cell leukemia/lymphoma (ATL) and a number of inflammatory diseases
These findings clearly suggest that both Tax sumoylation and nuclear body formation are not key determinants for Tax-mediated Nuclear factor-κB (NF-κB) activation
Some Tax and NF-κB essential modulator (NEMO) proteins within the signalsome are polyubiquitinated by the E2 ubiquitin conjugating enzyme and E3 ubiquitin ligase
Summary
Human T-cell lymphotropic virus type I (HTLV-I) is the etiological agent of adult T-cell leukemia/lymphoma (ATL) and a number of inflammatory diseases. It has been proposed that K63-linked polyubiquitination of Tax is critical for Tax-binding to NEMO and subsequent IKK activation and RelA nuclear translocation, while Tax sumoylation is required for the formation of Tax nuclear bodies and RelA-dependent transcription [9 and references therein].
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