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dc.contributor.authorLai, YuShuan (Cindy)
dc.contributor.authorRosenshine, Ilan
dc.contributor.authorLeong, John M.
dc.contributor.authorFrankel, Gad
dc.date2022-08-11T08:08:33.000
dc.date.accessioned2022-08-23T15:58:54Z
dc.date.available2022-08-23T15:58:54Z
dc.date.issued2013-11-01
dc.date.submitted2015-11-25
dc.identifier.citationCell Microbiol. 2013 Nov;15(11):1796-808. doi: 10.1111/cmi.12179. Epub 2013 Sep 3. <a href="http://dx.doi.org/10.1111/cmi.12179">Link to article on publisher's site</a>
dc.identifier.issn1462-5814 (Linking)
dc.identifier.doi10.1111/cmi.12179
dc.identifier.pmid23927593
dc.identifier.urihttp://hdl.handle.net/20.500.14038/30540
dc.description.abstractEnteropathogenic and enterohaemorrhagic Escherichia coli use a novel infection strategy to colonize the gut epithelium, involving translocation of their own receptor, Tir, via a type III secretion system and subsequent formation of attaching and effecting (A/E) lesions. Following integration into the host cell plasma membrane of cultured cells, and clustering by the outer membrane adhesin intimin, Tir triggers multiple actin polymerization pathways involving host and bacterial adaptor proteins that converge on the host Arp2/3 actin nucleator. Although initially thought to be involved in A/E lesion formation, recent data have shown that the known Tir-induced actin polymerization pathways are dispensable for this activity, but can play other major roles in colonization efficiency, in vivo fitness and systemic disease. In this review we summarize the roadmap leading from the discovery of Tir, through the different actin polymerization pathways it triggers, to our current understanding of their physiological functions.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=23927593&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC4036124/
dc.subject*Bacterial Adhesion
dc.subjectEnterohemorrhagic Escherichia coli
dc.subjectEnteropathogenic Escherichia coli
dc.subjectEpithelial Cells
dc.subject*Host-Pathogen Interactions
dc.subjectBacteriology
dc.subjectMicrobial Physiology
dc.subjectPathogenic Microbiology
dc.titleIntimate host attachment: enteropathogenic and enterohaemorrhagic Escherichia coli
dc.typeJournal Article
dc.source.journaltitleCellular microbiology
dc.source.volume15
dc.source.issue11
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/faculty_pubs/816
dc.identifier.contextkey7880392
html.description.abstract<p>Enteropathogenic and enterohaemorrhagic Escherichia coli use a novel infection strategy to colonize the gut epithelium, involving translocation of their own receptor, Tir, via a type III secretion system and subsequent formation of attaching and effecting (A/E) lesions. Following integration into the host cell plasma membrane of cultured cells, and clustering by the outer membrane adhesin intimin, Tir triggers multiple actin polymerization pathways involving host and bacterial adaptor proteins that converge on the host Arp2/3 actin nucleator. Although initially thought to be involved in A/E lesion formation, recent data have shown that the known Tir-induced actin polymerization pathways are dispensable for this activity, but can play other major roles in colonization efficiency, in vivo fitness and systemic disease. In this review we summarize the roadmap leading from the discovery of Tir, through the different actin polymerization pathways it triggers, to our current understanding of their physiological functions.</p>
dc.identifier.submissionpathfaculty_pubs/816
dc.contributor.departmentDepartment of Microbiology and Physiological Systems
dc.source.pages1796-808


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