Figure 3.
Figure 3. Effect of FXa and FXa inhibitors on transduction of HepG2 cells in vitro and liver transduction in vivo. HepG2 cells were transduced with AdCTL or AdKO1 (1000 VP/cell) in the presence of 1 IU/mL FX or FXa (A), 1 IU/mL active site-blocked Xa (FXa-EGR) (B), coincubated with 1 IU/mL FX and TAP at a molar ratio of 5.78:1 (TAP/FX) (C) or 2 μg/mL fondaparinux (D) for 3 hours, washed, and analyzed for β-galactosidase expression at 72 hours after infection. (E) Assessment of 100 μM PAR agonists on transduction by AdKO1. (F) Mice were given injections of AdKO1 in the absence or presence of pretreatment with fondaparinux (10 mg/kg intraperitoneally) and transgene expression in the liver assessed at 48 hours after infection. X-Gal-stained images are shown.

Effect of FXa and FXa inhibitors on transduction of HepG2 cells in vitro and liver transduction in vivo. HepG2 cells were transduced with AdCTL or AdKO1 (1000 VP/cell) in the presence of 1 IU/mL FX or FXa (A), 1 IU/mL active site-blocked Xa (FXa-EGR) (B), coincubated with 1 IU/mL FX and TAP at a molar ratio of 5.78:1 (TAP/FX) (C) or 2 μg/mL fondaparinux (D) for 3 hours, washed, and analyzed for β-galactosidase expression at 72 hours after infection. (E) Assessment of 100 μM PAR agonists on transduction by AdKO1. (F) Mice were given injections of AdKO1 in the absence or presence of pretreatment with fondaparinux (10 mg/kg intraperitoneally) and transgene expression in the liver assessed at 48 hours after infection. X-Gal-stained images are shown.

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