Department of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, PR China.
Virus Res. 2010 Jul;151(1):39-44. doi: 10.1016/j.virusres.2010.03.014. Epub 2010 Mar 31.
orf390 (WSSV449) is a novel apoptosis inhibitor gene in the genome of the White Spot Syndrome Virus (WSSV). In the present study, we focus on the function of orf390 gene. Stable expression of orf390 prevented SF9 insect cells from undergoing actinomycin D-induced apoptosis. ORF390 also rescued the replication of a p35-deficient-mutant (AcMNPVDeltap35k/pol+) in SF9 cells. In addition, ORF390 inhibits the activities of caspase-3 and -9 in vivo and in vitro. Here we demonstrate that the anti-apoptotic activity of ORF390 is dependent on two putative caspase-9 cleavage sites (VETD233 downward arrowG and LEHD303 downward arrowG) and one caspase-3 cleavage site (DEVD272 downward arrowG). Our results support the conclusion that these three sites play a key role in the suppression of apoptosis mediated by ORF390. These data further suggest that orf390 encodes a novel anti-apoptotic protein involved in cell survival and apoptosis regulation.
ORF390（WSSV449）是一种新型的凋亡抑制剂基因，位于白斑综合征病毒（WSSV）基因组中。在本研究中，我们专注于 ORF390 基因的功能。ORF390 的稳定表达可防止 SF9 昆虫细胞发生放线菌素 D 诱导的凋亡。ORF390 还可拯救 p35 缺失突变体（AcMNPVDeltap35k/pol+）在 SF9 细胞中的复制。此外，ORF390 在体内和体外抑制半胱天冬酶-3 和 -9 的活性。在这里，我们证明了 ORF390 的抗凋亡活性依赖于两个假定的半胱天冬酶-9 切割位点（VETD233 向下箭头 G 和 LEHD303 向下箭头 G）和一个半胱天冬酶-3 切割位点（DEVD272 向下箭头 G）。我们的结果支持以下结论：这三个位点在 ORF390 介导的凋亡抑制中起关键作用。这些数据进一步表明，orf390 编码一种新型的抗凋亡蛋白，参与细胞存活和凋亡调节。
