김은진
2019-05-23T04:40:24Z
2019-05-23T04:40:24Z
2017-03
JOURNAL OF MICROBIOLOGY AND BIOTECHNOLOGY, v. 27, No. 3, Page. 610-615
1017-7825
http://www.jmb.or.kr/journal/view.html?doi=10.4014/jmb.1611.11066
https://repository.hanyang.ac.kr/handle/20.500.11754/105890
When Shigella infect host cells, various effecter molecules are delivered into the cytoplasm of the host cell through the type III secretion system (TTSS) to facilitate their invasion process and control the host immune responses. Among these effectors, the S. flexneri effector OspF dephosphorylates mitogen- activated protein kinases and translocates itself to the nucleus, thus preventing histone H3 modification to regulate expression of proinflammatory cytokines. Despite the critical role of OspF, the mechanism by which it localizes in the nucleus has remained to be elucidated. In the present study, we identified a potential small ubiquitinrelated modifier (SUMO) modification site within OspF and we demonstrated that Shigella TTSS effector OspF is conjugated with SUMO in the host cell and this modification mediates the nuclear translocation of OspF. Our results show a bacterial virulence factor can exploit host post-translational machinery to execute its intracellular trafficking.
This work was supported by a research fund of Hanyang University (HY-2012-P).
en_US
KOREAN SOC MICROBIOLOGY & BIOTECHNOLOGY
Shigella flexneri
effector
OspF
SUMO
nuclear localization
Host Cell Nuclear Localization of Shigella flexneri Effector OspF Is Facilitated by SUMOylation
Article
3
27
10.4014/jmb.1611.11066
610-615
JOURNAL OF MICROBIOLOGY AND BIOTECHNOLOGY
Jo, Kyungmin
Kim, Eun Jin
Yu, Hyun Jin
Yun, Cheol-Heui
Kim, Dong Wook
2017006201
E
RESEARCH INSTITUTE[E]
INSTITUTE OF PHARMACEUTICAL SCIENCE AND TECHNOLOGY
ejkim0816