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Large tumor suppressor 2,LATS2,activates iNK in kinase-independent mechanism through ASK1

查看全文 作　　者：Lauren [1,2]Rusnak;Cong [2,3]Tang;Qi [2]Qi;Xiulei [2]Mo;Haian [1,2,4,5]Fu 高影响力作者 机构地区：[1]Graduate Program in Cancer Biology,Emory University,Atlanta,GA 30322,USA;[2]Department of Pharmacology and Emory Chemical Biology Discovery Center,Emory University,Atlanta,GA 30322,USA;[3]The First Affiliated Hospital,Medical School of Xi'an Jiaotong University,Xi'an 710061,China;[4]Winship Cancer Institute,Emory University,Atlanta,GA 30322,USA;[5]Department of Hematology and Medical Oncology,Emory University,Atlanta,GA 30322,USA高影响力机构 出　　处：《Journal of Molecular Cell Biology》索引2018年第10卷第6期,共10页高影响力期刊 摘　　要：Apoptosis signal-regulating kinase 1 (ASK1)is an important mediator of the cell stress response pathways.Because of its central role in regulating cell death,the activity of ASK1 is tightly regulated by protein-protein interactions and post-translational modifications.Deregulation of ASK1 activity has been linked to human diseases,such as neurological disorders and cancer.Here we describe the identification and characterization of large tumor suppressor 2 (LATS2)as a novel binding partner for ASK1.LATS2 is a core kinase in the Hippo signaling pathway and is commonly downregulated in cancer.We found that LATS2 interacts with ASK1 and increases ASK1-mediated signaUng to promote apoptosis and activate the iNK mitogen-activated protein kinase (MAPK).This change in MAPK signaling is dependent on the catalytic activity of ASK1 but does not require LATS2 kinase activity. This work identifies a novel role for LATS2 as a positive regulator of the ASK1-MKK-JNK signaling pathway and establishes a kinase-independent function of LATS2 that may be part of the intricate regulatory system for cellular response to diverse stress signals. 关 键 词：ASK1 LATS2 KINASE regulation signal TRANSDUCTION MITOGEN-ACTIVATED protein KINASE
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