Bacterial E3 Ubiquitin Ligase IpaH4.5 of Shigella flexneri Targets TBK1 To Dampen the Host Antibacterial Response.
Zheng, Zirui; Wei, Congwen; Guan, Kai; Yuan, Yuan; Zhang, Yanhong; Ma, Shengli; Cao, Ye; Wang, Fang; Zhong, Hui; He, Xiang.
; 196(3): 1199-208, 2016 Feb 01.
Artigo em Inglês | MEDLINE | ID: mdl-26700764
A Shigella effector dampens inflammation by regulating epithelial release of danger signal ATP through production of the lipid mediator PtdIns5P.
Structurally distinct bacterial TBC-like GAPs link Arf GTPase to Rab1 inactivation to counteract host defenses.
[SONNEI DYSENTERY MORBIDITY IN KHABAROVSK AND KHABAROVSK REGION DUE TO ATYPICAL MANNITOL-NEGATIVE CAUSATIVE AGENT].
A near death experience: Shigella manipulates host death machinery to silence innate immunity.
Septins restrict inflammation and protect zebrafish larvae from Shigella infection.
Towards a peptide-based vaccine against Shigella sonnei: A subtractive reverse vaccinology based approach.
Shigella Phages Isolated during a Dysentery Outbreak Reveal Uncommon Structures and Broad Species Diversity.
Shigella Effector OspB Activates mTORC1 in a Manner That Depends on IQGAP1 and Promotes Cell Proliferation.
The normal chain length distribution of the O antigen is required for the interaction of Shigella flexneri 2a with polarized Caco-2 cells.
Molecular mechanisms of host cytoskeletal rearrangements by Shigella invasins.