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A role for Taok2 in Listeria monocytogenes vacuolar escape.
The Journal of Infectious Diseases ( IF 6.4 ) Pub Date : 2020-06-25 , DOI: 10.1093/infdis/jiaa367
Juan J Quereda 1, 2 , Camille Morel 1 , Noelia Lopez-Montero 3, 4 , Jason Ziveri 5, 6 , Steven Rolland 1 , Théodore Grenier 7 , Nathalie Aulner 8 , Anne Danckaert 8 , Alain Charbit 5, 6 , Jost Enninga 3, 4 , Pascale Cossart 1 , Javier Pizarro-Cerdá 9
Affiliation  

The bacterial pathogen Listeria monocytogenes (Lm) invades host cells, ruptures its internalization vacuole and reaches the cytosol for replication. A high-content siRNA microscopy screen allowed us to identify epithelial cell factors involved in Lm vacuolar rupture, among them the serine/threonine kinase Taok2. Kinase activity inhibition using a specific drug validated a role for Taok2 in favoring Lm cytoplasmic access. Furthermore, we showed that Taok2 recruitment to Lm vacuoles requires the presence of pore-forming toxin listeriolysin O. Overall, our study identifies the first set of host factors modulating Lm vacuolar rupture and cytoplasmic access in epithelial cells.

中文翻译:

Taok2 在李斯特菌液泡逃逸中的作用。

细菌病原体单核细胞增生李斯特菌( Lm ) 侵入宿主细胞,破坏其内化液泡并到达细胞质进行复制。高含量 siRNA 显微镜筛选使我们能够识别参与Lm液泡破裂的上皮细胞因子,其中包括丝氨酸/苏氨酸激酶 Taok2。使用特定药物抑制激酶活性验证了 Taok2 在有利于Lm细胞质进入方面的作用。此外,我们表明,Taok2 向Lm液泡的募集需要存在成孔毒素李斯特菌溶血素 O。总的来说,我们的研究确定了第一组调节上皮细胞中Lm液泡破裂和细胞质进入的宿主因子。
更新日期:2020-06-27
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