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Nathan R. Brady

Researcher at Johns Hopkins University

Publications -  53
Citations -  15731

Nathan R. Brady is an academic researcher from Johns Hopkins University. The author has contributed to research in topics: Autophagy & Mitochondrion. The author has an hindex of 30, co-authored 52 publications receiving 13485 citations. Previous affiliations of Nathan R. Brady include University Hospital Heidelberg & Heidelberg University.

Papers
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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

Phosphorylation of the Autophagy Receptor Optineurin Restricts Salmonella Growth

Philipp Wild, +13 more
- 08 Jul 2011 - 
TL;DR: It is proposed that phosphorylation of autophagy receptors might be a general mechanism for regulation of cargo-selectiveautophagy, resulting in increased intracellular bacterial proliferation.
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Response to myocardial ischemia/reperfusion injury involves Bnip3 and autophagy.

Anne Hamacher-Brady, +7 more
- 01 Jan 2007 - 
TL;DR: The results suggest that Bnip3 contributes to I/R injury which triggers a protective stress response with upregulation of autophagy and removal of damaged mitochondria.
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Enhancing Macroautophagy Protects against Ischemia/Reperfusion Injury in Cardiac Myocytes

Anne Hamacher-Brady, +2 more
- 06 Oct 2006 - 
TL;DR: It is found that autophagic flux is impaired at the level of both induction and degradation and that enhancing autophagy constitutes a powerful and previously uncharacterized protective mechanism against I/R injury to the heart cell.