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Negative regulation of interferon-gamma/STAT1 signaling through cell adhesion and cell density-dependent STAT1 dephosphorylation

文献类型：期刊论文

作者Chen, Zhimin1; Ma, Xiuquan2; Zhang, Haohao1; Sun, Xiaoxiao1; Shen, Shensi1; Li, Ying2; Gu, Yuan1; Wang, Ying1; Yan, Shoushen1; Yu, Qiang1
刊名CELLULAR SIGNALLING
出版日期2011-08
卷号23期号:8页码:1404-1412
关键词STAT Interferon-gamma T-cell protein tyrosine phosphatase Extracellular matrix Actin cytoskeleton Tyrosine dephosphorylation
ISSN号0898-6568
DOI10.1016/j.cellsig.2011.04.003
文献子类Article
英文摘要Signal transducer and activator of transcription 1 (STAT1) is an important mediator for cytokine signal transduction, particularly IFN-gamma. Following IFN-gamma stimulation, STAT1 is activated through tyrosine phosphorylation. Little is known about the function and regulation of STAT1 dephosphorylation after activation. We studied the regulation and function of STAT1 dephosphorylation in different types of cells and found that the phosphorylated STAT1 was quickly dephosphorylated in most of epithelial cells. Further studies revealed that the dephosphorylation of STAT1 was regulated by cell shape/adhesion. Actin cytoskeleton and extracellular matrix (ECM) proteins mediated the STAT1 dephosphorylation through the T-cell protein tyrosine phosphatase TCPTP. Inactivation of the dephosphorylation system by cell detachment rendered the cells more sensitive to IFN-gamma-induced cell death. Our results revealed a novel mechanism in regulating IFN-gamma/STAT1 signaling. This cell adhesion and cell cytoskeleton-dependent STAT1 dephosphorylation system may have a role in IFN-gamma-mediated immunosurveillance for cancer cells by inducing anoikis of detached metastatic cancer cells. (C) 2011 Elsevier Inc. All rights reserved.
WOS关键词PROTEIN-TYROSINE-PHOSPHATASE ; INTERFERON-GAMMA RECEPTOR ; APOPTOSIS-INDUCING LIGAND ; MHC CLASS-I ; IFN-GAMMA ; INHIBITORY FACTOR ; TUMOR-METASTASIS ; T-CELLS ; GROWTH ; ACTIVATION
资助项目China National Natural Science Foundation[30672481] ; China National Natural Science Foundation[30771097] ; China National Natural Science Foundation[90713029] ; China National Natural Science Foundation[30828018] ; Shanghai Science and Technology Research Grant[08DZ1971403] ; Shanghai Science and Technology Research Grant[09JC1416700] ; China Ministry of Science and Technology[2008ZX10002-020] ; National Science & Technology Major Project "Key New Drug Creation and Manufacturing Program", China[2009ZX09301-001] ; National Science & Technology Major Project "Key New Drug Creation and Manufacturing Program", China[2009ZX09103-064]
WOS研究方向Cell Biology
语种英语
WOS记录号WOS:000291509700020
出版者ELSEVIER SCIENCE INC
源URL[http://119.78.100.183/handle/2S10ELR8/278467]  
专题药理学第一研究室
通讯作者Yu, Qiang
作者单位1.Chinese Acad Sci, Shanghai Inst Mat Med, Shanghai 201203, Peoples R China;
2.Chinese Acad Sci, Shanghai Inst Organ Chem, Shanghai 201203, Peoples R China
推荐引用方式
GB/T 7714		 Chen, Zhimin,Ma, Xiuquan,Zhang, Haohao,et al. Negative regulation of interferon-gamma/STAT1 signaling through cell adhesion and cell density-dependent STAT1 dephosphorylation[J]. CELLULAR SIGNALLING,2011,23(8):1404-1412.
APA Chen, Zhimin.,Ma, Xiuquan.,Zhang, Haohao.,Sun, Xiaoxiao.,Shen, Shensi.,...&Yu, Qiang.(2011).Negative regulation of interferon-gamma/STAT1 signaling through cell adhesion and cell density-dependent STAT1 dephosphorylation.CELLULAR SIGNALLING,23(8),1404-1412.
MLA Chen, Zhimin,et al."Negative regulation of interferon-gamma/STAT1 signaling through cell adhesion and cell density-dependent STAT1 dephosphorylation".CELLULAR SIGNALLING 23.8(2011):1404-1412.

入库方式： OAI收割

来源：上海药物研究所

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