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. 2023 Jul 5;120(28):e2219475120. doi: 10.1073/pnas.2219475120

Fig. 3.

Fig. 3.

The defect in Gag processing imposed by disruption of nSMase2 is not due to impaired GagPol incorporation into virions. (A) 293T cells were transfected with pNL4-3 or the PR-defective derivative pNL4-3/PR(−) and 8 h posttransfection, cells were treated with 0, 5, and 10 µM PDDC or 10 µM inactive control compound (Cntrl). Twenty-four hours posttransfection, cell and virus lysates were prepared and subjected to western blot analysis with HIV-Ig as in Fig. 1A or anti-HIV PR antibody. (B) 293T cells were transduced with lentiviral particles carrying scrambled (Scr) or nSMase2 (nSM)-specific siRNA as in Fig. 1E and 24 h posttransduction, cells were transfected with WT pNL4-3 or the PR-defective derivative pNL4-3/PR(−), and virus lysates were prepared and subjected to western blot analysis as in Fig. 3A. The mobility of molecular mass standards is shown on the left of each blot in kDa. The positions of GagPol, Pr55, p49, p41, p24, and PR are labeled on the right. A representative image from two independent experiments is shown.