通过刺激β-catenin依赖转录,PGK1增强了生产性牛性疹病毒1感染
Xuan Li1, Wenyuan Gu2, Shitao Li3
1Key Laboratory of Microbial Diversity Research and Application of Hebei Province, School of Life Sciences, Hebei University, Baoding, 071002, China.
Veterinary research
|March 7, 2025
概括
牛疹病毒1 (BoHV-1) 感染增加了线粒体糖酸酶1 (PGK1) 蛋白. 通过促进活性β-catenin的核积累,PGK1信号增强了BoHV-1的复制.
科学领域:
- 病毒学 病毒学
- 分子生物学分子生物学
- 生物化学 生化学
背景情况:
- 牛疹病毒1 (BoHV-1) 生产性感染利用β-catenin依赖的转录进行复制.
- 糖酸酶1 (PGK1) 对于ATP产生至关重要,并与组织损伤有关.
- 在BoHV-1复制中PGK1信号传递的确切作用尚不清楚.
研究的目的:
- 调查BoHV-1复制和PGK1信号传递之间的关系.
- 阐明PGK1影响病毒复制和致病性的机制.
主要方法:
- 在BoHV-1感染期间研究了PGK1蛋白在线粒体中的积累.
- 分析了β-catenin和PGK1表达水平之间的相互作用.
- 评估了PGK1对β-catenin依赖的转录活性和核定位的影响.
主要成果:
- 感染BoHV-1显著增加了线粒体PGK1蛋白水平.
- β-catenin和PGK1对彼此的蛋白质表达有互惠的调节作用,在感染过程中反转.
- PGK1促进了受感染细胞中活性β-catenin和-β-catenin (S552) 的核积累,增强了病毒复制.
结论:
- PGK1信号传递在促进BoHV-1复制方面发挥着重要作用.
- 通过调节β-catenin活性,PGK1可能有助于BoHV-1的致病性.
- 这项研究揭示了PGK1和病毒复制机制之间的新联系.
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