Pseudo Rabies Virus Protein UL34 Interacted with UL31 to Disrupt the Human Lamin A

Pseudo Rabies Virus Protein UL34 Interacted with UL31 to Disrupt the Human Lamin A
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伪狂犬病病毒蛋白 UL34 与 UL31 相互作用破坏人核纤层蛋白 A

DOI:
10.1007/s11859-018-1347-5
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发表时间:
2018-10
影响因子:
--
通讯作者:
JI Shaoping
JI Shaoping
中科院分区:
--
文献类型:
--
作者:
WEI Wenqiang;HU Zichao;KANG Xiaonan;WANG Xuan;WANG Hongju;JI Shaoping

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伪狂犬病病毒 (PRV) 通过从内核膜 (INM) 出芽而从细胞核中逸出。核层在 INM 下方形成中间丝的刚性网状结构。目前尚不清楚 PRV 感染是否会引起椎板破坏。在本文中,可以观察到核纤层蛋白A在PRV感染期间发生断裂。 UL34 位于核边缘,但 UL31 在细胞核中积累为不同的斑块。有趣的是,在 UL34 存在的情况下,UL31 的一部分定位于 INM。免疫沉淀 (IP) 测定证实 PRV UL31 和 UL34 在转染细胞中相互作用。重要的是,UL31 和 UL34 的共表达直接破坏了核纤层蛋白 A,类似于 PRV 感染期间观察到的情况。总之,PRV感染诱导Lamin A的破坏,而UL34和UL31在Lamin A的破坏中发挥着关键作用。
Pseudo rabies virus (PRV) egresses from the nucleus by budding from the inner nuclear membrane (INM). The nuclear lamina forms a rigid meshwork of intermediate filaments underlying the INM. It remains unknown whether PRV infection induces the disruption of lamina. In this paper, it can be observed that nuclear Lamin A became fractured during PRV infection. UL34 was localized at the nuclear rim, but UL31 was accumulated in the nucleus as distinct patches. Interestingly, a part of UL31 was localized at the INM in the presence of UL34. Immunoprecipitation (IP) assay confirmed that PRV UL31 and UL34 interacted in the transfected cells. Importantly, the co-expression of UL31 and UL34 directly disrupted Lamin A, resembling that observed during PRV infection. In conclusion, PRV infection induces the disruption of Lamin A, and UL34 and UL31 play a critical role in the disruption of Lamin A.
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发表时间: 1998-07
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