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Young H. Lee

Researcher at National Institutes of Health

Publications -  36
Citations -  5903

Young H. Lee is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Signal transduction & Hepatocyte growth factor. The author has an hindex of 15, co-authored 31 publications receiving 5392 citations. Previous affiliations of Young H. Lee include Uniformed Services University of the Health Sciences.

Papers
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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.
Journal ArticleDOI

The microtubule plus-end localization of Aspergillus dynein is important for dynein−early-endosome interaction but not for dynein ATPase activation

Jun Zhang, +5 more
- 15 Oct 2010 - 
TL;DR: It is shown in Aspergillus nidulans that kinesin-1-dependent plus-end localization is not a prerequisite for dynein ATPase activation, and it is suggested that the normal ability of dyenin to interact with microtubules as an active minus-end-directed motor demands kinesIn1-mediated plus- end accumulation for effective interactions with early endosomes.
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Englerin A Stimulates PKCθ to Inhibit Insulin Signaling and to Simultaneously Activate HSF1: Pharmacologically Induced Synthetic Lethality

Carole Sourbier, +11 more
- 11 Feb 2013 - 
TL;DR: By promoting glucose addiction, while simultaneously starving cells of glucose, EA proves to be synthetically lethal to highly glycolytic tumors.
Journal Article

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

Daniel J. Klionsky, +2459 more
- 01 Jan 2016 - 
Journal ArticleDOI

Angiotensin-II-induced apoptosis requires regulation of nucleolin and Bcl-xL by SHP-2 in primary lung endothelial cells

Young H. Lee, +4 more
- 15 May 2010 - 
TL;DR: Findings suggest that nucleolin is a primary target of Ang-II signaling, and thatAng-II-activated SHP-2 inhibits nucleolin binding to Bcl-xL mRNA, thus affecting the equilibrium between pro- and anti-apoptotic members of the B cl-2 family.