PRL-3 dephosphorylates p38 MAPK to promote cell survival under stress.

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作者： Yin,Shi ^[1] ; Shengfeng,Xu ^[2] ; Natalie Y L,Ngoi ^[3] ; Qi,Zeng ^[4] ; Zu,Ye ^[5]

作者单位： Department of Immunology, Zhejiang University School of Medicine, Hangzhou, 310058, China; Department of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, 119077, Singapore. Electronic address: yinshi@zju.edu.cn. ^[1] Department of Genetics, The University of Texas MD Anderson Cancer Center, Houston, 77030, USA. ^[2] Department of Investigational Cancer Therapeutics, Division of Cancer Medicine, The University of Texas MD Anderson Cancer Center, Houston, 77030, USA; Department of Hematology-Oncology, National University Cancer Institute, 119228, Singapore. ^[3] Institute of Molecular and Cell Biology, A*STAR Agency for Science Technology and Research, 138673, Singapore; Department of Biochemistry, Yong Loo Lin School of Medicine, National University of Singapore, 119260, Singapore. Electronic address: mcbzengq@imcb.a-star.edu.sg. ^[4] Department of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, 119077, Singapore; Institute of Molecular and Cell Biology, A*STAR Agency for Science Technology and Research, 138673, Singapore; Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, Houston, 77030, USA. Electronic address: zye4@mdanderson.org. ^[5]

关键词 Apoptosis Hypoxia PRL-3 Phosphatase ROS Tumor microenvironment p38 MAPK