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. 2010 Dec 23;22(10):1225–1237. doi: 10.1089/hum.2010.012

FIG. 1.

FIG. 1.

The expression of R88-APOBEC3G (R88-A3G) mutants and their resistance to Vif-mediated degradation. (A) Schematic representation of R88-A3G mutants at the cytidine deaminase activity site (E259Q), viral packaging site (P124A), and Vif-response site (D128K, P129A). (B and C) R88-A3G wild-type or mutant expressors were co-transfected with a pcDNA-hVif expressor in 293T cells. At 48-hr post-transfection, cells were pulse-radiolabeled with [35S]-methionine for 30 min and collected and lysed at 0, 3.5, and 5 hr. The level of R88-A3Gwt/mutant in each lysed cell sample was evaluated by anti-Vpr immunoprecipitation (upper panel). The level of degradation of wild-type and mutant R88-A3G was quantified by laser densitometry (lower panel). The result shown is representative of two independent experiments.