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Lan N. Tu

Researcher at Cornell University

Publications -  19
Citations -  742

Lan N. Tu is an academic researcher from Cornell University. The author has contributed to research in topics: Translocator protein & Medicine. The author has an hindex of 10, co-authored 14 publications receiving 605 citations. Previous affiliations of Lan N. Tu include Ithaca College & University of Washington.

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Peripheral benzodiazepine receptor/translocator protein global knock-out mice are viable with no effects on steroid hormone biosynthesis.

TL;DR: In an attempt to correlate the in vivo findings to previously used in vitro models, it is determined that siRNA knockdown or the absence of TSPO in different mouse and human steroidogenic cell lines had no effect on steroidogenesis.
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Identification of Michael Acceptor-Centric Pharmacophores with Substituents That Yield Strong Thioredoxin Reductase Inhibitory Character Correlated to Antiproliferative Activity

TL;DR: Identification of Michael acceptor-centric pharmacophores among diversified compounds demonstrates that a systematic approach to discover and develop Michaelacceptor-based TrxR inhibitors is feasible.
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PK11195 effect on steroidogenesis is not mediated through the translocator protein (TSPO).

TL;DR: Results show that the pharmacological effect of PK11195 on steroidogenesis is not mediated through TSPO, and both control and control MA-10:Tspo+/+ cells responded in a similar dose-dependent manner showing increases in progesterone production.
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Translocator Protein (TSPO) Affects Mitochondrial Fatty Acid Oxidation in Steroidogenic Cells

TL;DR: Results demonstrate the first experimental evidence that TSPO can affect mitochondrial energy homeostasis through modulation of FAO, a function that appears to be consistent with high levels of TSPo expression observed in cell types active in lipid storage/metabolism.
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Metabolomic characteristics of cholesterol-induced non-obese nonalcoholic fatty liver disease in mice.

TL;DR: Gas- and liquid chromatography/mass spectrometry-based profiling of lipidomic and primary metabolism changes in the liver and plasma revealed that systemic mechanisms leading to steatosis and hepatitis in this non-obese NAFLD model were driven by a combination of effects directed by elevated free cholesterol, cholesterol esters and cholic acid, and associated changes to metabolism of sphingomyelins and phosphatidylcholines.