Department of Molecular Biology, Princeton University, Lewis Thomas Laboratory, Princeton, New Jersey, USA.
J Virol. 2013 May;87(10):6044-6. doi: 10.1128/JVI.00129-13. Epub 2013 Mar 13.
Although several adenovirus type 5 (Ad5) proteins prevent deleterious consequences of activation of p53, it has been reported that viral replication proceeds more efficiently when human tumor cells produce wild-type compared to mutant p53. We have now exploited RNA interference and lentiviral vectors to achieve essentially complete knockdown of p53 in normal human cells: no effects on the kinetics or efficiency of viral gene expression or production of infectious particles were observed.
虽然几种 5 型腺病毒(Ad5)蛋白可防止 p53 激活产生的有害后果,但据报道,当人肿瘤细胞产生野生型而非突变型 p53 时,病毒复制会更有效率。我们现在利用 RNA 干扰和慢病毒载体,在正常的人类细胞中实现了对 p53 的基本完全敲低:未观察到对病毒基因表达或感染性颗粒产生的动力学或效率有任何影响。