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Teresa L. M. Thurston

Researcher at Imperial College London

Publications -  34
Citations -  8361

Teresa L. M. Thurston is an academic researcher from Imperial College London. The author has contributed to research in topics: Innate immune system & Autophagy. The author has an hindex of 18, co-authored 28 publications receiving 7319 citations. Previous affiliations of Teresa L. M. Thurston include Medical Research Council & Laboratory of Molecular Biology.

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Journal ArticleDOI

Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

Daniel J. Klionsky, +2522 more
- 21 Jan 2016 - 
TL;DR: In this paper, the authors present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macro-autophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
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Galectin 8 targets damaged vesicles for autophagy to defend cells against bacterial invasion

Teresa L. M. Thurston, +4 more
- 16 Feb 2012 - 
TL;DR: It is shown in human cells that galectin 8 (also known as LGALS8), a cytosolic lectin, is a danger receptor that restricts Salmonella proliferation and serves as a versatile receptor for vesicle-damaging pathogens.
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The TBK1 adaptor and autophagy receptor NDP52 restricts the proliferation of ubiquitin-coated bacteria.

Teresa L. M. Thurston, +5 more
- 11 Oct 2009 - 
TL;DR: It is concluded that human cells utilize the ubiquitin system and NDP52 to activate autophagy against bacteria attempting to colonize their cytosol.
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Salmonella SPI-2 Type III Secretion System Effectors: Molecular Mechanisms And Physiological Consequences.

Elliott Jennings, +2 more
- 09 Aug 2017 - 
TL;DR: The biochemical activities, host cell interaction partners, and physiological functions of SPI-2 T3SS effectors are summarized in the context of the selective pressures encountered by S. enterica in vivo to achieve a unified understanding of how effector activities work together to promote Salmonella virulence.
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Salmonella persisters undermine host immune defenses during antibiotic treatment

Daphne A.C. Stapels, +8 more
- 07 Dec 2018 - 
TL;DR: It is shown that Salmonella persisters arising during macrophage infection maintain a metabolically active state, which may confer an advantage to the pathogen during relapse once antibiotic pressure is relieved.