纽卡斯尔病病毒通过Src激活各种信号通路,以促进病毒进入宿主巨细胞
Qiankai Shi1, Ran Zhao1, Linna Chen1
1Division of Avian Infectious Diseases, State Key Laboratory of Animal Disease Control and Prevention, Harbin Veterinary Research Institute, the Chinese Academy of Agricultural Sciences, Harbin, China.
Journal of virology
|February 9, 2024
概括
纽卡斯尔病病毒 (NDV) 进入细胞使用化物作为受体,触发Src信号为洞穴介导的内细胞分裂. 这一途径涉及诸如caveolin-1和dynamin-2之类的关键蛋白质,协调病毒的进入.
科学领域:
- 细胞生物学 细胞生物学
- 病毒学 病毒学
- 病毒进入的分子机制.
背景情况:
- 洞穴介导的内细胞分裂 (CavME) 是一种细胞内化过程.
- 像纽卡斯尔病病毒 (NDV) 这样的病原体利用CavME进入.
- 由于NDV诱导的CavME的分子机制尚未完全理解.
研究的目的:
- 通过CavME阐明NDV通过宿主细胞进入宿主细胞的分子机制.
- 为了确定特定的受体和信号通路参与NDV诱导的内细胞分裂.
- 为帕拉米克索病毒进入机制提供新的见解.
主要方法:
- 研究了NDV与细胞表面受体的结合 (类蛋白与葡萄糖蛋白).
- 分析了 Src 激酶在 NDV 进入和蛋白质酸化 (Cav1,Dyn2) 中的作用.
- 检查了Rho GTPases (RhoA,Cdc42) 和actin细胞骨架重组的参与.
主要成果:
- NDV使用含有酸的化物,而不是糖蛋白,作为受体.
- 结合NDV激活Src酶,导致Cav1和Dyn2酸化,这对内细胞分裂至关重要.
- 对RhoA和Cdc42的Src-依赖激活调节了NDV进入的actin细胞骨动态.
结论:
- NDV的进入是由化物结合和随后的Src激活信号介导的.
- 这个过程涉及洞穴相关蛋白质 (Cav1,Dyn2) 和Rho GTPases.
- 这项研究揭示了NDV内细胞进入宿主细胞的新型分子机制.
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