| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 8268489 | Free Radical Biology and Medicine | 2015 | 13 Pages |
Abstract
- FGF9-induced HO-1 and γ-GCS expression was prevented by an FGFR inhibitor, PD173014.
- FGF9 induced ERK and AKT phosphorylation and CREB and Nrf2 activation in neurons.
- ERK or AKT inhibition prevented FGF9 antioxidative functions and neuroprotection.
- Knockdown of CREB or Nrf2 blocked FGF9 functions, but not ERK and AKT activity.
- FGF9-induced HO-1 and γ-GCS upregulation is mediated by the FGFR/ERK, AKT/CREB and Nrf2 signaling pathway.
Keywords
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Authors
Jih-Ing Chuang, Jui-Yen Huang, Shaw-Jenq Tsai, H. Sunny Sun, Shang-Hsun Yang, Pei-Chin Chuang, Bu-Miin Huang, Cheng-Hsin Ching,