Yeh C T, Wong S W, Fung Y K, Ou J H
Department of Microbiology, University of Southern California, Los Angeles 90033.
Proc Natl Acad Sci U S A. 1993 Jul 15;90(14):6459-63. doi: 10.1073/pnas.90.14.6459.
The hepatitis B virus (HBV) core protein has been found in the nucleus, the cytoplasm, or both of HBV-infected hepatocytes. However, the mechanism that regulates the subcellular localization of the HBV core protein is still unclear. In this report, we demonstrate that nuclear localization of the HBV core protein is cell cycle-regulated in two different cell lines. The amount of the core protein in the nucleus was increased during the G1 phase, reduced to an undetectable level during the S phase, and increased again when the cells were confluent and ceased to grow. Thus, the nuclear localization of the core protein during HBV infection can be at least partially attributed to liver injury and regeneration, which cause the hepatocytes to enter cell cycles. Based on the observation that the cytoplasmic core protein was phosphorylated and the nuclear core protein was not, we speculate that nuclear localization of the HBV core protein is negatively regulated by phosphorylation during the cell cycle.
乙型肝炎病毒（HBV）核心蛋白已在HBV感染的肝细胞的细胞核、细胞质或两者中被发现。然而，调节HBV核心蛋白亚细胞定位的机制仍不清楚。在本报告中，我们证明了HBV核心蛋白的核定位在两种不同的细胞系中受细胞周期调控。细胞核中核心蛋白的量在G1期增加，在S期降至不可检测水平，当细胞汇合并停止生长时再次增加。因此，HBV感染期间核心蛋白的核定位至少部分可归因于肝损伤和再生，这导致肝细胞进入细胞周期。基于细胞质核心蛋白被磷酸化而细胞核核心蛋白未被磷酸化的观察结果，我们推测HBV核心蛋白的核定位在细胞周期中受到磷酸化的负调控。
