Laakkonen P, Auvinen P, Kujala P, Kääriäinen L
Institute of Biotechnology, Viikki Biocenter, University of Helsinki, Helsinki, Finland.
J Virol. 1998 Dec;72(12):10265-9. doi: 10.1128/JVI.72.12.10265-10269.1998.
Expression of the NSP1 protein of Semliki Forest virus and Sindbis virus in cultured cells induced filopodia-like extensions containing NSP1 but not F actin. The actin stress fibers disappeared, whereas vimentin, keratin, and tubulin networks remained intact. The effects of NSP1 were dependent on its palmitoylation but not on its enzymatic activities and were also observed in virus-infected cells.
塞姆利基森林病毒和辛德毕斯病毒的NSP1蛋白在培养细胞中的表达诱导了含有NSP1但不含F肌动蛋白的丝状伪足样延伸。肌动蛋白应力纤维消失，而波形蛋白、角蛋白和微管蛋白网络保持完整。NSP1的作用取决于其棕榈酰化而非其酶活性，并且在病毒感染的细胞中也观察到了这些作用。
