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• W2160090062 abstract "ABSTRACT Salmonella enterica encodes a type III secretion system (TTSS) within a pathogenicity island located at centisome 63 (SPI-1), which is essential for its pathogenicity. This system mediates the transfer of a battery of bacterial proteins into the host cell with the capacity to modulate cellular functions. The transfer process is dependent on the function of protein translocases SipB, SipC, and SipD. We report here that Salmonella protein InvE, which is also encoded within SPI-1, is essential for the translocation of bacterial proteins into host cells. An S. enterica serovar Typhimurium mutant carrying a loss-of-function mutation in invE shows reduced secretion of SipB, SipC, and SipD while exhibiting increased secretion of other TTSS effector proteins. We also demonstrate that InvE interacts with a protein complex formed by SipB, SipC, and their cognate chaperone, SicA. We propose that InvE controls protein translocation by regulating the function of the Sip protein translocases." @default.
• W2160090062 created "2016-06-24" @default.
• W2160090062 creator A5016995233 @default.
• W2160090062 creator A5067255009 @default.
• W2160090062 date "2002-09-01" @default.
• W2160090062 modified "2023-09-23" @default.
• W2160090062 title "<i>Salmonella</i> Type III Secretion-Associated Protein InvE Controls Translocation of Effector Proteins into Host Cells" @default.
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• W2160090062 doi "https://doi.org/10.1128/jb.184.17.4699-4708.2002" @default.
• W2160090062 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/135284" @default.
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