B
B. Brett Finlay
Researcher at University of British Columbia
Publications - 609
Citations - 69318
B. Brett Finlay is an academic researcher from University of British Columbia. The author has contributed to research in topics: Virulence & Effector. The author has an hindex of 135, co-authored 588 publications receiving 61894 citations. Previous affiliations of B. Brett Finlay include Vaccine and Infectious Disease Organization & Canadian Institute for Advanced Research.
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Journal ArticleDOI
Characteristics of Helicobacter pylori attachmentto human primary antral epithelial cells
Ursula Heczko,Ursula Heczko,Valerie C. Smith,R Mark Meloche,Alison M.J. Buchan,B. Brett Finlay +5 more
TL;DR: It is concluded that bacterial shape conversion, adherence and secretion of outer membrane vesicles are features of H. pylori infection.
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Bacterial Disease in Diverse Hosts
TL;DR: Hueck et al. as discussed by the authors showed that the University of British Columbia also transport specific virulence factors directly into Vancouver, British Columbia host cells, acting as a syringe to deliver these factors Canada V6T 1Z3 into the host cell cytoplasm or membrane.
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Putting E. coli on a pedestal: a unique system to study signal transduction and the actin cytoskeleton.
TL;DR: The mechanism of infection and pedestal formation is discussed and how this system might be a powerful tool for studying actin dynamics at the plasma membrane.
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The pathogenic Escherichia coli type III secreted protease NleC degrades the host acetyltransferase p300
Stephanie R. Shames,Amit P. Bhavsar,Matthew A. Croxen,Robyn J. Law,Stefanie H. C. Mak,Wanyin Deng,Yuling Li,Roza Bidshari,Carmen L. de Hoog,Leonard J. Foster,B. Brett Finlay +10 more
TL;DR: This work has identified a second target of NleC and provided the first example of a bacterial virulence factor targeting the acetyltransferase p300, and demonstrated that overexpression of p300 can antagonize repression of IL‐8 secretion by EPEC and that siRNA knock‐down of p 300 dampens IL‐ 8 secretion byEPEC ΔnleC‐infected cells.
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Helicobacter pylori infection targets adherens junction regulatory proteins and results in increased rates of migration in human gastric epithelial cells.
Victoria S. Conlin,Susan B. Curtis,Ying Zhao,Edwin D.W. Moore,Valerie C. Smith,R. Mark Meloche,B. Brett Finlay,Alison M.J. Buchan +7 more
TL;DR: A correlation between H. pylori infection and alterations to epithelial cell adhesion molecules, including increased levels of Rho-GTP and cell migration is demonstrated, indicating that destabilizing epithelialcell adherence is one of the factors increasing the risk of H.pylori-infected individuals developing gastric cancer.