伪狂犬病病毒US3蛋白激酶介导肌动蛋白应激纤维的分解。
Pseudorabies virus US3 protein kinase mediates actin stress fiber breakdown.
作者信息
Van Minnebruggen Geert, Favoreel Herman W, Jacobs Liesbeth, Nauwynck Hans J
机构信息
Laboratory of Virology, Faculty of Veterinary Medicine, Ghent University, 9820 Merelbeke, Belgium.
出版信息
J Virol. 2003 Aug;77(16):9074-80. doi: 10.1128/jvi.77.16.9074-9080.2003.
Abstract
Disruption of specific components of the host cytoskeleton has been reported for several viruses and is thought to be beneficial for viral replication and spread. Our previous work demonstrated that infection of swine kidney (SK-6) cells with pseudorabies virus (PRV), a swine alphaherpesvirus, induced actin stress fiber breakdown. In the present study, using several PRV deletion mutants, we found that the US3 serine/threonine (S/T) protein kinase is involved in breakdown of actin stress fibers in different PRV-infected cell lines. Further, by transfection assays, we showed that PRV US3 itself, in the absence of other viral proteins, is able to trigger actin stress fiber breakdown when it is localized in sufficient amounts in the nucleus.
摘要
据报道，几种病毒会破坏宿主细胞骨架的特定成分，并且认为这对病毒的复制和传播有益。我们之前的研究表明，猪α疱疹病毒伪狂犬病病毒（PRV）感染猪肾（SK-6）细胞会导致肌动蛋白应激纤维断裂。在本研究中，我们使用几种PRV缺失突变体，发现US3丝氨酸/苏氨酸（S/T）蛋白激酶参与了不同PRV感染细胞系中肌动蛋白应激纤维的断裂。此外，通过转染试验，我们表明，在没有其他病毒蛋白的情况下，当PRV US3在细胞核中足够量定位时，它能够触发肌动蛋白应激纤维的断裂。
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