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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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Signal transduction between enteropathogenic Escherichia coli (EPEC) and epithelial cells: EPEC induces tyrosine phosphorylation of host cell proteins to initiate cytoskeletal rearrangement and bacterial uptake

TL;DR: In this article, enteropathogenic Escherichia coli (EPEC) induces assembly of a complex cytoskeletal structure within the eucaryotic cell, localized beneath the adherent bacterium.
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When a pandemic and an epidemic collide: COVID-19, gut microbiota, and the double burden of malnutrition.

TL;DR: In this article, the authors discuss how COVID-19 may indirectly exacerbate the double burden of malnutrition (DBM) through food insecurity and the gut microbiome, and suggest that providing access to nutritious foods and protecting individuals' gut microbiome to "flatten the curve" of the DBM trajectory should be prioritized.
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SepD/SepL-Dependent Secretion Signals of the Type III Secretion System Translocator Proteins in Enteropathogenic Escherichia coli

TL;DR: It is shown that the secreted T3SS components, the translocators, and both LEE- and non-LEE-encoded effectors all carry N-terminal type III secretion and translocation signals, and it is suggested that the secretion hierarchy of the different substrates is determined by a signal other than the N-Terminal secretion signal.
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Protective Role of Akt2 in Salmonella enterica Serovar Typhimurium-Induced Gastroenterocolitis

TL;DR: The differences in bacterial loads and cecal inflammation in WT and Akt2 KO mice infected with WT Salmonella were abolished when these mice were infected with the sopB deletion mutant, indicating that SopB may play a role in protecting the mice from Salmoneella infection through the activation of Akt1.