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dc.contributor.authorHallstrom, Kelly N.
dc.contributor.authorMcCormick, Beth A.
dc.date2022-08-11T08:08:56.000
dc.date.accessioned2022-08-23T16:12:57Z
dc.date.available2022-08-23T16:12:57Z
dc.date.issued2016-04-15
dc.date.submitted2017-09-13
dc.identifier.citation<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>
dc.identifier.issn1949-0976 (Linking)
dc.identifier.doi10.1080/19490976.2015.1128626
dc.identifier.pmid27078059
dc.identifier.urihttp://hdl.handle.net/20.500.14038/33506
dc.description.abstractSalmonella 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.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=27078059&dopt=Abstract">Link to Article in PubMed</a></p>
dc.rights© 2016 Kelly N. Hallstrom and Beth A. McCormick.
dc.subjectSalmonella
dc.subjecthost pathogen interactions
dc.subjectinflammation
dc.subjecttrafficking
dc.subjecttype III secretion
dc.subjectImmunology and Infectious Disease
dc.subjectMicrobiology
dc.titleThe type three secreted effector SipC regulates the trafficking of PERP during Salmonella infection
dc.typeJournal Article
dc.source.journaltitleGut microbes
dc.source.volume7
dc.source.issue2
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=3053&amp;context=gsbs_sp&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/gsbs_sp/2030
dc.identifier.contextkey10740187
refterms.dateFOA2022-08-23T16:12:57Z
html.description.abstract<p>Salmonella 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.</p>
dc.identifier.submissionpathgsbs_sp/2030
dc.contributor.departmentDepartment of Microbiology and Physiological Systems
dc.source.pages136-45
dc.contributor.studentKelly N. Hallstrom


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