Encouragingly, transient expression of the full prenylation mutant (Rap1b-CAAX) accelerated virus infection in a highly significant dose-dependent manner, even higher by about 33% at a 0.5 μg transfection amount than the Rap1b (AA) mutant with a 3 μg transfection amount, which broke the limit of wild-type Rap1b’s promoting effect on virus infection at a high transfection dose ( Figure 2 E).
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ICP4-Associated Activation of Rap1b Facilitates Herpes Simplex Virus Type I (HSV-1) Infection in Human Corneal Epithelial Cells.
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Furthermore, the PKA agonist Forskolin disturbed Rap1b activation in a dose-dependent manner, accompanied by a decreasing trend in viral infection.