Hallstrom, Kelly N.McCormick, Beth A.2022-08-232022-08-232016-04-152017-09-13<p>Gut Microbes. 2016;7(2):136-45. doi: 10.1080/19490976.2015.1128626. <a href="https://doi.org/10.1080/19490976.2015.1128626">Link to article on publisher's site</a></p>1949-0976 (Linking)10.1080/19490976.2015.112862627078059https://hdl.handle.net/20.500.14038/33506Salmonella enterica Typhimurium employs type III secreted effectors to induce cellular invasion and pathogenesis. We previously reported the secreted effector SipA is in part responsible for inducing the apical accumulation of the host membrane protein PERP, a host factor we have shown is key to the inflammatory response induced by Salmonella. We now report that the S. Typhimurium type III secreted effector SipC significantly contributes to PERP redistribution to the apical membrane surface. To our knowledge, this is the first report demonstrating a role for SipC in directing the trafficking of a host membrane protein to the cell surface. In sum, facilitation of PERP trafficking appears to be a result of type III secreted effector-mediated recruitment of vesicles to the apical surface. Our study therefore reveals a new role for SipC, and builds upon previous reports suggesting recruitment of vesicles to the cell surface is important for Salmonella invasion.en-US© 2016 Kelly N. Hallstrom and Beth A. McCormick.Salmonellahost pathogen interactionsinflammationtraffickingtype III secretionImmunology and Infectious DiseaseMicrobiologyJournal Articlehttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=3053&amp;context=gsbs_sp&amp;unstamped=1https://escholarship.umassmed.edu/gsbs_sp/203010740187gsbs_sp/2030