Fig. 7: Test of virion packaging and antiviral activity of rA3G and hA3G mutants designed to disrupt the binding to AA dinucleotide RNA.
From: Structural basis of sequence-specific RNA recognition by the antiviral factor APOBEC3G

a, b Surface representation of rA3G showing locations of six mutational groups (mutants 1–6). c Predicted function of mutants 1–6 for rA3G and hA3G. The mutated residues are identical in rA3G and hA3G except mutant 6, where rA3G has A187E/T188E, and hA3G has I187E/M188E. d–f The results of virion packaging of rA3G mutants and their restriction of HIV-1 infectivity using HIV-1(ΔVif). g–i The results of virion packaging of hA3G mutants and their restriction of HIV-1 infectivity using HIV-1(ΔVif). The virion packaging results are quantified as results of duplicate independent experiments (n = 2) and the restriction of HIV-1 infectivity assays are presented as results of triplicated independent experiments (n = 3). All graphs shown in Fig. 7 are represented as mean values ± SD. j Representative gel images of EMSA using the 6-FAM labeled RNA3-AA (10 nM) and the purified wild-type rA3GR8 or six rA3G mutant proteins of various concentrations (1.4, 4.1, 12.3, 37, 111, 333, 1000, and 2000 nM). n = 3 independent experiments. The asterisk marks the location of 6-FAM. Source data are provided as a Source Data file.