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

Fig 3

MAVS selectively stabilizes vFLIP.

(A) Immunoblots of extracts of 293T cells transfected with non- or V5-tagged viral and cellular FLIPs along with empty or Flag-MAVS vectors for 24 h. Red asterisks indicate bands of expected molecular weight. (B) Immunoblots of extracts from WT and MAVS KO 293T cells transfected with V5-vFLIP and either empty vector or Flag-MAVS and incubated in EBSS and complete media (–EBSS) for 6 h. Relative V5-vFLIP intensities normalized to β-actin were noted under each band. (C) Real time-quantitative PCR analysis of V5-vFLIP mRNA expression. Total RNAs were isolated from the cells transfected and treated as in (B) above. Data are represented as mean ± SD of triplicate samples. (**p<0.05) (D) Immunoblots of extracts from WT and MAVS KO 293T cells transfected with V5-vFLIP and either empty vector or Flag-MAVS and treated with cycloheximide (CHX) for 0, 1, 2, and 3 h. “Endo.MAVS” indicates endogenous MAVS. (E) Immunoblots of extracts from 293T cells transfected with vFLIP and either empty vector or Flag-MAVS and treated with DMSO or 1 μM PU-H71 for 24 h.

Fig 3

doi: https://doi.org/10.1371/journal.ppat.1007058.g003