phosphatidylinositol 3-kinase (PI3K )-AKT 小径涉及各种各样的细胞的功能,包括骑车的 anti-apoptosis,蛋白质合成,葡萄糖新陈代谢和房间。然而,在甲壳纲的动物的 PI3K-AKT 小径的角色仍然保持不清楚。在现在的学习,我们从 Litopenaeus vannamei 克隆并且描绘 AKT 基因 lvakt。511 残余 LVAKT 高度被保存;包含了一个 PH 领域,一个催化领域和一个恐水病的领域;并且高度在 L 的心和鳃被表示。vannamei。我们发现用实时量的 PCR (Q-PCR ) 分析,那 lvakt 在早白色期间是起来调整的点症候群病毒(WSSV ) 感染。而且, PI3K 特定的禁止者, LY294002,减少的病毒的基因抄写,暗示 PI3K-AKT 小径可能被 WSSV 劫持。我们的结果因此建议 LVAKT 可以对 WSSV 在虾免疫者反应起一个重要作用。
The phosphatidylinositol 3-kinase (PI3K)-AKT pathway is involved in various cellular functions, including anti-apoptosis, protein synthesis, glucose metabolism and cell cycling. However, the role of the PI3K-AKT pathway in crustaceans remains unclear. In the present study, we cloned and characterized the AKT gene lvakt from Litopenaeus vannamei. The 511-residue LVAKT was highly conserved; contained a PH domain, a catalytic domain and a hydrophobic domain; and was highly expressed in the heart and gills of L. vannamei. We found, using Real-Time Quantitative PCR (Q-PCR) analysis, that lvakt was up- regulated during early white spot syndrome virus (WSSV) infection. Moreover, the PI3K-specific inhibitor, LY294002, reduced viral gene transcription, implying that the PI3K-AKT pathway might be hijacked by WSSV. Our results therefore suggest that LVAKT may play an important role in the shrimp immune response against WSSV.