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. 2011 Dec;85(23):12482–12491. doi: 10.1128/JVI.05218-11

Fig. 3.

Fig. 3.

A dominant-negative Cul5 mutant and a C-terminal hydrophilic replacement ElonginC mutant can both disrupt the activity of FIV Vif against fA3s. (A) CrFK cells (106) were cotransfected with 100 ng of VR-fA3Z3-HA, VR-fA3Z2-Z3-HA, or VR-fA3Z2a-HA and 400 ng of VR-FIV Vif-myc or VR1012, adjusted to 700 ng with 200 ng of VR-hCul5ΔNedd8, a control vector VR-hCul1K720R or VR1012. The cells were harvested 48 h after transfection and analyzed by Western blotting with anti-HA, anti-myc, and anti-tubulin antibodies. The percentages of fA3s in the presence of Cul5 ΔNedd8 were calculated relative to that in the absence of FIV Vif (set to 100%). (B) CrFK cells (106) were cotransfected with 100 ng of VR-fA3Z3-HA, VR-fA3Z2-Z3-HA, or VR-fA3Z2a-HA and 400 ng of VR-FIV Vif-myc or VR1012, adjusted to 700 ng with 200 ng of fElonginC WT-HA, fElonginC Δ2-HA, or VR1012. The cells were harvested 48 h after transfection and analyzed by Western blotting with anti-HA, anti-myc and anti-tubulin antibodies. The percentages of fA3s in the presence of ElonginCΔ2 were calculated relative to that in the absence of FIV Vif (set to 100%).