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Timothy C. Barnett

Researcher at University of Queensland

Publications -  41
Citations -  3751

Timothy C. Barnett is an academic researcher from University of Queensland. The author has contributed to research in topics: Streptococcus pyogenes & Innate immune system. The author has an hindex of 24, co-authored 41 publications receiving 3173 citations. Previous affiliations of Timothy C. Barnett include Telethon Institute for Child Health Research & University of Western Australia.

Papers
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Journal ArticleDOI

Pathogenesis of group A streptococcal infections.

TL;DR: A vaccine capable of preventing GAS infection may be the only effective way to control and eliminate G AS infection and disease.
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Disease Manifestations and Pathogenic Mechanisms of Group A Streptococcus

TL;DR: Genomic and molecular analyses have now characterized a large number of GAS virulence determinants, many of which exhibit overlap and redundancy in the processes of adhesion and colonization, innate immune resistance, and the capacity to facilitate tissue barrier degradation and spread within the human host.
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Molecular insight into invasive group A streptococcal disease

TL;DR: The virulence factors and newly discovered molecular events that mediate the in vivo changes from non-invasive GAS serotype M1T1 to the invasive phenotype are described and the invasive-disease trigger for non-M1 GAS is reviewed.
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Surface Proteins of Gram-Positive Bacteria and How They Get There

TL;DR: The structure of the cell surface is the major characteristic that distinguishes gram-positive from gram-negative bacteria, and the processes used to transport and attach these proteins show significant differences between these bacterial classes.
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FANTOM5 CAGE profiles of human and mouse samples

Shuhei Noguchi, +185 more
- 29 Aug 2017 - 
TL;DR: In the FANTOM5 project, transcription initiation events across the human and mouse genomes were mapped at a single base-pair resolution and their frequencies were monitored by CAGE coupled with single-molecule sequencing to represent the consequence of transcriptional regulation in each analyzed state of mammalian cells.