Fig. 6
From: HTLV-1 Tax plugs and freezes UPF1 helicase leading to nonsense-mediated mRNA decay inhibition
Model proposed for Tax-mediated inhibition of UPF1 activity. The fate of UPF1 depends on the time frame of interaction with Tax that occurs during HTLV-1 infection. Tax can prevent the recruitment of UPF1 to the RNA substrate. Alternately, Tax can affect the activity of previously bound RNA and NMD-engaged UPF1: the translocation activities of UPF1 can be blocked by Tax binding. The UPF1/Tax complex then dissociates from the RNA substrate or remains stuck in P-bodies
