Title |
Glycogen synthase kinase-3β inactivation inhibits tumor necrosis factor-α production in microglia by modulating nuclear factor κB and MLK3/JNK signaling cascades
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Published in |
Journal of Neuroinflammation, December 2010
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DOI | 10.1186/1742-2094-7-99 |
Pubmed ID | |
Authors |
Mei-Jen Wang, Hsin-Yi Huang, Wu-Fu Chen, Hui-Fen Chang, Jon-Son Kuo |
Abstract |
Deciphering the mechanisms that modulate the inflammatory response induced by microglial activation not only improves our insight into neuroinflammation but also provides avenues for designing novel therapies that could halt inflammation-induced neuronal degeneration. Decreasing glycogen synthase kinase-3β (GSK-3β) activity has therapeutic benefits in inflammatory diseases. However, the exact molecular mechanisms underlying GSK-3β inactivation-mediated suppression of the inflammatory response induced by microglial activation have not been completely clarified. Tumor necrosis factor-α (TNF-α) plays a central role in injury caused by neuroinflammation. We investigated the regulatory effect of GSK-3β on TNF-α production by microglia to discern the molecular mechanisms of this modulation. |
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Geographical breakdown
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Demographic breakdown
Readers by professional status | Count | As % |
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Student > Ph. D. Student | 16 | 20% |
Student > Master | 13 | 16% |
Researcher | 9 | 11% |
Student > Doctoral Student | 6 | 8% |
Student > Bachelor | 6 | 8% |
Other | 9 | 11% |
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Readers by discipline | Count | As % |
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Pharmacology, Toxicology and Pharmaceutical Science | 5 | 6% |
Other | 10 | 13% |
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