Research Article, Cell Biol Henderson Nv Vol: 5 Issue: 2
YAP, A Component of the Hippo Pathway, is Essential for Antioxidant Defense
| Song Fu1, Renhua Lv2, Haitao Hou1, Longqiang Wang1, Haijun Liu1, Huan Wang1, Xiangpeng Huang1, Yanan Wang1 and Shize Shao1* | |
| 1Department of Spine and Spinal Cord Surgery, Wendeng Orthopeadic Hospital, Weihai, Shandong, 264400, PR China | |
| 2Department of Neurology, the Affiliated Weihai Central Hospital of Weifang Medical College, Weihai, Shandong, 264400, PR China | |
| Corresponding author : Shize Shao
Department of Spine and Spinal Cord Surgery, Wendeng Orthopeadic Hospital, No. 1 Fengshan Road, Wengdeng District, Weihai City, Shangdong Province, 264400, China Tel: +86 0631-8487208 Fax: +86 0631-8453115 E-mail: Shao.shize@gmail.com |
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| Received: April 08, 2016 Accepted: June 06, 2016 Published: June 11, 2016 | |
| Citation: Fu S, Lv R, Hou H, Wang L, Liu H, et al. (2016) YAP, A Component of the Hippo Pathway, is Essential for Antioxidant Defense. Cell Biol (Henderson, NV) 5:2. doi:10.4172/2324-9293.1000125 |
Abstract
The highly conserved Hippo signaling pathway which negatively regulates cell growth and survival is a key regulator of organ size and tumorigenesis. Emerging evidence suggests the important role of Hippo pathway in response to oxidative stress. However the mechanism was rarely explored. Here we reported that YAP protein, which is the terminal effector of Hippo signaling pathway, shuttled between cytoplasm and nucleus following different concentration of sodium arsenite treatment, thereby controlling cell death or survival under arsenite-induced oxidative stress. Low concentration of sodium arsenite inhibited phosphorylation of YAP S127 and promoted YAP translocation to nucleus, thus further enhanced cell proliferation. However, high concentration of sodium arsenite augmented phosphorylation of YAP at S127 and induced translocation of YAP into cytoplasm and further caused cell apoptosis. These results suggest that YAP translocation plays an important role in deciding cell fate under arsenite-induced oxidative stress.
