在细胞进入过程中,WAVE1和WAVE2促进了由人类乳头瘤病毒驱动的活性蛋白聚合
D J Fernandez1, Stephanie Cheng1, Ruben Prins1
1Department of Molecular Microbiology & Immunology and Norris Comprehensive Cancer Center, University of Southern California, Los Angeles, CA, United States.
bioRxiv : the preprint server for biology
|November 18, 2024
概括
威斯科特-阿尔德里奇综合征蛋白WAVE1和WAVE2对于人类乳头瘤病毒16型 (HPV16) 感染至关重要. 这些蛋白质调解了actin重组,促进HPV16通过filopodia形成进入上皮细胞.
科学领域:
- 细胞生物学 细胞生物学
- 病毒学 病毒学
- 分子生物学分子生物学
背景情况:
- 人类乳头瘤病毒16型 (HPV16) 导致人体癌症,并且需要内细胞分裂才能感染.
- 通过HPV16触发细胞进入的actin重组的确切机制尚不清楚.
研究的目的:
- 调查威斯科特-阿尔德里奇综合征蛋白质家族1号和2号维普罗林同类蛋白 (WAVE1和WAVE2) 在HPV16内细胞化中的作用.
- 为了阐明HPV16细胞表面相互作用如何启动由actin驱动的内细胞分裂.
主要方法:
- 转录后基因沉默和基因组编辑以评估WAVE1和WAVE2的功能.
- 同焦点光显微镜用于分析HPV16,WAVE1,WAVE2和actin的局部化.
- 在修改了WAVE蛋白水平的细胞中量化HPV16内化率.
主要成果:
- WAVE1和WAVE2对于有效的HPV16感染至关重要;它们的缺失显著减少了HPV16的内部化.
- 在淘汰细胞中恢复WAVE1或WAVE2可以挽救HPV16感染.
- HPV16,WAVE1,WAVE2和actin在细胞背面进行同位化,HPV16通过WAVE1和WAVE2.2的介导刺激了类动物的形成.
结论:
- WAVE1和WAVE2是HPV16内细胞化所需的活性蛋白聚合的关键分子媒介.
- 感染HPV16的控制方式是通过将actin重组成filopodial突起来控制,这是由WAVE1和WAVE2.2介导的过程.
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