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Patty J. Lee

Researcher at Duke University

Publications -  142
Citations -  15835

Patty J. Lee is an academic researcher from Duke University. The author has contributed to research in topics: Lung injury & Hyperoxia. The author has an hindex of 48, co-authored 131 publications receiving 14144 citations. Previous affiliations of Patty J. Lee include Yale University & Walter Reed Army Institute of Research.

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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.
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Regulation of lung injury and repair by Toll-like receptors and hyaluronan.

Dianhua Jiang, +15 more
- 23 Oct 2005 - 
TL;DR: It is reported that hyaluronan degradation products require MyD88 and both Toll-like receptor (TLR)4 and TLR2 in vitro and in vivo to initiate inflammatory responses in acute lung injury and epithelial cell apoptosis after lung injury.
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Hypoxia-inducible Factor-1 Mediates Transcriptional Activation of the Heme Oxygenase-1 Gene in Response to Hypoxia

Patty J. Lee, +6 more
- 28 Feb 1997 - 
TL;DR: Data demonstrate that hypoxia induces HO-1 expression in animal tissues and cell cultures and implicate HIF-1 in this response.
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Overexpression of heme oxygenase-1 in human pulmonary epithelial cells results in cell growth arrest and increased resistance to hyperoxia

Patty J. Lee, +3 more
- 17 Sep 1996 - 
TL;DR: The data suggest that overexpression of HO-1 results in cell growth arrest, which may facilitate cellular protection against non-heme-mediated oxidant insult such as hyperoxia.
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Early Growth Response Gene 1–mediated Apoptosis Is Essential for Transforming Growth Factor β1–induced Pulmonary Fibrosis

Chun Geun Lee, +11 more
- 02 Aug 2004 - 
TL;DR: It is demonstrated that Egr-1–mediated apoptosis is a prerequisite for TGF-β1–induced fibrosis and remodeling and defined the critical role of Egr–1 in the TGF–β1 phenotype.