Nakahara Tomomi, Nishimura Akiko, Tanaka Masakazu, Ueno Takaharu, Ishimoto Akinori, Sakai Hiroyuki
Laboratory of Gene Analysis, Department of Viral Oncology, Institute for Virus Research, Kyoto University, Sakyo-Ku, Kyoto 606-8507, Japan.
J Virol. 2002 Nov;76(21):10914-20. doi: 10.1128/jvi.76.21.10914-10920.2002.
The life cycle of human papillomaviruses (HPVs) is tightly coupled to the differentiation program of their host epithelial cells. HPV E4 gene expression is first observed in the parabasal layers of squamous epithelia, suggesting that the E4 gene product contributes to the mechanism of differentiation-dependent virus replication, although its biological function remains unclear. We analyzed the effect of HPV type 18 E4 on cell proliferation and found that E4 expression induced cell cycle arrest at the G(2)/M boundary. The functional region of E4 necessary for the growth arrest activity was located in the central portion of the molecule, and this activity was independent of the E4-mediated collapse of cytokeratin intermediate filament structures.
人乳头瘤病毒（HPV）的生命周期与其宿主上皮细胞的分化程序紧密相连。HPV E4基因的表达最初在鳞状上皮的副基底层中被观察到，这表明E4基因产物有助于依赖分化的病毒复制机制，尽管其生物学功能仍不清楚。我们分析了18型HPV E4对细胞增殖的影响，发现E4表达诱导细胞周期在G(2)/M边界处停滞。E4生长停滞活性所需的功能区域位于分子的中央部分，并且该活性独立于E4介导的细胞角蛋白中间丝结构的解体。
