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Jian Dong

Researcher at Research Triangle Park

Publications -  7
Citations -  1295

Jian Dong is an academic researcher from Research Triangle Park. The author has contributed to research in topics: Gene silencing & Transcription factor. The author has an hindex of 7, co-authored 7 publications receiving 1122 citations. Previous affiliations of Jian Dong include Wuhan University of Science and Technology & COMSATS Institute of Information Technology.

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Recent advances in 2D and 3D in vitro systems using primary hepatocytes, alternative hepatocyte sources and non-parenchymal liver cells and their use in investigating mechanisms of hepatotoxicity, cell signaling and ADME.

Patricio Godoy, +94 more
TL;DR: This review encompasses the most important advances in liver functions and hepatotoxicity and analyzes which mechanisms can be studied in vitro and how closely hepatoma, stem cell and iPS cell–derived hepatocyte-like-cells resemble real hepatocytes.
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CNC-bZIP Protein Nrf1-Dependent Regulation of Glucose-Stimulated Insulin Secretion

TL;DR: A novel role of Nrf1 is demonstrated in regulating glucose metabolism and insulin secretion in β-cells and NRF1 is characterized as a key transcription factor that regulates the coupling of glycolysis and mitochondrial metabolism and GSIS.
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Regulatory role of KEAP1 and NRF2 in PPARγ expression and chemoresistance in human non-small-cell lung carcinoma cells

TL;DR: In this article, a stable knockdown of Kelch-like ECH-associated protein 1 (KEAP1) by lentiviral shRNA sensitized three independent NSCLC cell lines to multiple chemotherapeutic agents, including arsenic trioxide (As(2)O(3)), etoposide, and doxorubicin, despite moderately increased NRF2 levels.
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Long isoforms of NRF1 negatively regulate adipogenesis via suppression of PPARγ expression.

TL;DR: The findings in the present study provide further evidence for a novel role of NRF1 beyond its participation in cellular antioxidant response and suggest that L-NRF1 is a negative regulator of PPARγ2 expression and thereby can suppress adipogenesis.