在HSV-1pUL37蛋白质通过调节kinesin-1电机促进细胞入侵
DongHo Kim1, Michael A Cianfrocco2, Kristen J Verhey3
1Department of Microbiology-Immunology, Northwestern University Feinberg School of Medicine, Chicago, IL 60611.
概括
简单疹病毒1型 (HSV-1) 使用pUL37蛋白来抑制细胞入侵期间的kinesin-1运动活性. 这种调节对于病毒传输和神经侵袭至关重要.
科学领域:
- 病毒学 病毒学
- 细胞生物学 细胞生物学
- 神经科学是一个神经科学.
背景情况:
- 像HSV-1这样的神经型阿尔法赫珀病毒,利用宿主细胞机械进行入侵.
- 病毒颗粒在进入细胞时通过微管子运动蛋白进行运输.
研究的目的:
- 研究HSV-1 pUL37体蛋白在病毒细胞进入过程中调节素-1运动功能的作用.
- 阐明pUL37在逆行轴突运输过程中抑制kinesin-1的机制.
主要方法:
- 研究了感染细胞中的HSV-1pUL37和kinesin-1之间的相互作用.
- 利用蛋白质表达和局部化研究来确定功能域.
- 评估了pUL37对素-1活性和病毒贩运的影响.
主要成果:
- 在逆行轴突运输过程中,HSV-1 pUL37抑制了基因素-1 电机.
- 对于这种抑制,pUL37的区域2 (R2) 是必要的.
- 动力域和近端卷状卷的kinesin-1是足够的病毒同化和pUL37介导的抑制.
结论:
- 在空间和时间上,HSV-1 pUL37调节了基因素-1的活动.
- 调节发生在进入病毒粒子的背景下,通过kinesin-1的氨基末端运动区域进行.
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