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Paul S. Brookes

Researcher at University of Rochester Medical Center

Publications -  190
Citations -  26488

Paul S. Brookes is an academic researcher from University of Rochester Medical Center. The author has contributed to research in topics: Mitochondrion & Cardioprotection. The author has an hindex of 61, co-authored 183 publications receiving 23122 citations. Previous affiliations of Paul S. Brookes include University of Birmingham & University of Cambridge.

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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.
Journal ArticleDOI

Guidelines for the use and interpretation of assays for monitoring autophagy

Daniel J. Klionsky, +1287 more
- 01 Apr 2012 - 
TL;DR: These guidelines are presented for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
Journal ArticleDOI

Calcium, ATP, and ROS: a mitochondrial love-hate triangle

Paul S. Brookes, +4 more
- 01 Oct 2004 - 
TL;DR: A "two-hit" hypothesis is developed, in which Ca(2+) plus another pathological stimulus can bring about mitochondrial dysfunction, and the delicate balance between the positive and negative effects of Ca( 2+) and the signaling events that perturb this balance is highlighted.
Journal ArticleDOI

Ischaemic accumulation of succinate controls reperfusion injury through mitochondrial ROS.

Edward T. Chouchani, +29 more
- 20 Nov 2014 - 
TL;DR: In this article, a comparative in vivo metabolomic analysis was conducted to identify widely conserved metabolic pathways responsible for mitochondrial reactive oxygen species (ROS) production during ischaemia reperfusion.
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BCL-2 inhibition targets oxidative phosphorylation and selectively eradicates quiescent human leukemia stem cells.

Eleni D. Lagadinou, +13 more
- 07 Mar 2013 - 
TL;DR: This work evaluated mechanisms controlling oxidative state in primary specimens derived from acute myelogenous leukemia (AML) patients and proposed a model wherein the unique physiology of ROS-low LSCs provides an opportunity for selective targeting via disruption of BCL-2-dependent oxidative phosphorylation.