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Peroxisomes support human herpesvirus 8 latency by stabilizing the viral oncogenic protein vFLIP via the MAVS-TRAF complex

Fig 6

MAVS promotes K63-linked polyubiquitination at lysine 118 of vFLIP.

(A) Diagram of the single and combined vFLIP mutations in lysine residues at positions 13, 46, and 118. (B) Immunoblots of extracts from WT and MAVS KO 293T cells transfected for 24 h with expression vectors for WT V5-vFLIP and the indicated mutants of V5-vFLIP. (C) In vivo vFLIP ubiquitination assays using 293T cells transfected with vectors expressing WT or lysine-mutated V5-vFLIP with or without Flag-MAVS in the presence of 10 μM MG-132 for 24 h.

Fig 6