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. 2018 Sep 14;430(18Part B):3111–3128. doi: 10.1016/j.jmb.2018.06.052

Fig. 5.

Fig. 5

DDX17 utilizes distinct RNA binding motifs. (a) Schematic representation of DDX17 and the annotated individual point mutations that are defective for the glycine doublet function and RNA/ATPase binding activities. HeLa M cells were sequentially transfected with siControl or siRNA targeting DDX17 (siDDX17 with or without increasing concentrations of siDDX17-resistant DDX17–T253R + E255V + L256A; siDDX17-resistant DDX17–S356L; siDDX17-resistant DDX17–R508Q or siDDX17-resistant G280D). (b) Effect on HIV-1 relative virus production following endogenous DDX17 depletion and rescue with DDX17–T253R + E255V + L256A. (c) Western blot showing DDX17 knockdown and rescue with DDX17–T253R + E255V + L256A. (d) Effect on HIV-1 relative virus production following DDX17 knockdown and rescue with DDX17–T301D. (e) Western blot showing DDX17 knockdown and rescue with DDX17–T301D. (f) Effect on HIV-1 relative virus production following DDX17 knockdown and rescue with DDX17–S356L. (g) Effect on HIV-1 relative virus production following DDX17 knockdown and rescue with DDX17–R508Q. (h) Western blot showing DDX17 knockdown and rescue with DDX17–S356L. (i) Western blot showing DDX17 knockdown and rescue with DDX17–R508Q. (j) Effect on HIV-1 relative virus production following DDX17 knockdown and rescue with DDX17–G280D. (k) Western blot showing DDX17 knockdown and rescue with DDX17–G280D. Each graph is a representative of two independent experiments done in triplicate. Bars represent mean of triplicate samples ± SEM. Statistical significance *P < 0.05, **P < 0.01.