Research Topics
| A T MaurelliSummaryAffiliation: Uniformed Services University of the Health Sciences Country: USA Publications
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Detail Information
Publications
"Black holes" and bacterial pathogenicity: a large genomic deletion that enhances the virulence of Shigella spp. and enteroinvasive Escherichia coliA T Maurelli
Department of Microbiology and Immunology, Uniformed Services University of the Health Sciences, F Edward Hebert School of Medicine, Bethesda, MD 20814 4799, USA
Proc Natl Acad Sci U S A 95:3943-8. 1998..Thus, understanding the role of black holes in pathogen evolution may yield clues to new treatments of infectious diseases...
Pathoadaptive mutations that enhance virulence: genetic organization of the cadA regions of Shigella sppW A Day
Department of Microbiology and Immunology, F Edward Hebert School of Medicine, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814 4799, USA
Infect Immun 69:7471-80. 2001..These observations strongly support the role of pathoadaptive mutation as an important pathway in the evolution of pathogenic organisms...
Establishment of unipolar localization of IcsA in Shigella flexneri 2a is not dependent on virulence plasmid determinantsR C Sandlin
Department of Microbiology and Immunology, F Edward Hebert School of Medicine, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814 4799, USA
Infect Immun 67:350-6. 1999..The unipolar localization of IcsA in the E. coli background suggests that a common pathway that allows IcsA to be spatially restricted to one pole on the bacterial cell surface exists in Shigella and E. coli...
Spa33, a cell surface-associated subunit of the Mxi-Spa type III secretory pathway of Shigella flexneri, regulates Ipa protein trafficR Schuch
Department of Microbiology and Immunology, , Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814, USA
Infect Immun 69:2180-9. 2001..These findings indicate that Spa33 is a mobile element within Mxi-Spa, which is required to control Ipa translocation into and out of OM positions of the secretory structure...
MxiM and MxiJ, base elements of the Mxi-Spa type III secretion system of Shigella, interact with and stabilize the MxiD secretin in the cell envelopeR Schuch
Department of Microbiology and Immunology, , Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814-4799, USA
J Bacteriol 183:6991-8. 2001....
Avirulence of rough mutants of Shigella flexneri: requirement of O antigen for correct unipolar localization of IcsA in the bacterial outer membraneR C Sandlin
Department of Microbiology and Immunology, F Edward Hebert School of Medicine, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814 4799
Infect Immun 63:229-37. 1995..These observations indicate a more precise role for LPS in Shigella pathogenesis...
Inhibition of Shigella flexneri-induced transepithelial migration of polymorphonuclear leucocytes by cadaverineB A McCormick
Department of Pediatric Gastroenterology and Nutrition, Massachusetts General Hospital East, Charlestown 02129, USA
Cell Microbiol 1:143-55. 1999..coli (EPEC) to induce PMN migration. These observations not only provide insight into mechanisms of S. flexneri pathogen evolution and pathogenesis, but also suggest a potential for the use of cadaverine in the treatment of dysentery...
Temperature regulation of Shigella virulence: identification of the repressor gene virR, an analogue of hns, and partial complementation by tyrosyl transfer RNA (tRNA1(Tyr))A E Hromockyj
Department of Microbiology, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814 4799
Mol Microbiol 6:2113-24. 1992..These data constitute the first direct genetic evidence that virR is an analogue of the E. coli hns gene, and suggest a model for temperature regulation of Shigella species virulence via the bacterial translational machinery...
mxiA of Shigella flexneri 2a, which facilitates export of invasion plasmid antigens, encodes a homolog of the low-calcium-response protein, LcrD, of Yersinia pestisG P Andrews
Department of Microbiology, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814 4799
Infect Immun 60:3287-95. 1992..We conclude that mxiA is a homolog of the Y. pestis lcrD locus and may function similarly in S. flexneri, either by directly affecting the excretion of virulence factors or by regulating the expression of export accessory genes...
