Simple jQuery Dropdowns
Please use this identifier to cite or link to this item:
Full metadata record
DC FieldValueLanguage
dc.contributor.authorSariqa Wagleyen_US
dc.contributor.authorMuthita Vanapornen_US
dc.contributor.authorDarawan Rinchaien_US
dc.contributor.authorLaura Conejeroen_US
dc.contributor.authorGanjana Lertmemongkolchaien_US
dc.contributor.authorGregory J. Bancroften_US
dc.contributor.authorRichard W. Titballen_US
dc.contributor.otherUniversity of Exeteren_US
dc.contributor.otherMahidol Universityen_US
dc.contributor.otherKhon Kaen Universityen_US
dc.contributor.otherLondon School of Hygiene & Tropical Medicineen_US
dc.identifier.citationMicrobial Pathogenesis. Vol.107, (2017), 175-180en_US
dc.description.abstract© 2017 Elsevier Ltd The NRPS/PKS cluster encodes the enzymes necessary for glidobactin synthesis it is partially conserved in various members of the Burkholderia genus including B. pseudomallei. In this study we have shown that the insertional inactivation or deletion of glbC in this cluster in B. pseudomallei could reduce the ability of the bacterium to survive or grow in murine macrophages or in human neutrophils. Exogenously added proteasome inhibitors were able to chemically complement the mutation. The insertional inactivation or deletion of glbC increased virulence in an acute model of infection in Balb/c or C57BL/6 mice but virulence in a chronic model of infection was similar to that of the wild type. Our findings contrast with the previous finding that inactivation of the glb gene cluster in B. pseudomallei strain 1026b resulted in marked attenuation, and provides evidence of differential roles for some genes in virulence of different strains of B. pseudomallei.en_US
dc.rightsMahidol Universityen_US
dc.subjectImmunology and Microbiologyen_US
dc.titleA proteasome inhibitor produced by Burkholderia pseudomallei modulates intracellular growthen_US
Appears in Collections:Scopus 2016-2017

Files in This Item:
There are no files associated with this item.

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.