USP38 critically promotes asthmatic pathogenesis by stabilizing JunB protein
2018-11
发表期刊JOURNAL OF EXPERIMENTAL MEDICINE (IF:12.6[JCR-2023],14.1[5-Year])
ISSN0022-1007
卷号215期号:11页码:2850-2867
发表状态已发表
DOI10.1084/jem.20172026
摘要Th2 immune response is critical for allergic asthma pathogenesis. Molecular mechanisms for regulating Th2 immunity are still not well understood. Here we report that the ubiquitin-specific protease USP38 is crucial for Th2-mediated allergic asthma. TCR stimulation up-regulated the USP38 level, and USP38 in turn mediated the protein stabilization of JunB, a transcription factor specific for Th2 development. Consequently, USP38 was specifically required for TCR-induced production of Th2 cytokines and Th2 development both in vitro and in vivo, and USP38-deficient mice were resistant to asthma pathogenesis induced by OVA or HDM. Mechanistically, USP38 directly associated with JunB, deubiquitinated Lys-48-linked poly-ubiquitination of JunB, and consequently blocked TCR-induced JunB turnover. USP38 represents the first identified deubiquitinase specifically for Th2 immunity and the associated asthma.
收录类别SCI ; SCIE
语种英语
资助项目Strategic Priority Research Program of the Chinese Academy of Sciences[XDB19000000]
WOS研究方向Immunology ; Research & Experimental Medicine
WOS类目Immunology ; Medicine, Research & Experimental
WOS记录号WOS:000449278300014
出版者ROCKEFELLER UNIV PRESS
WOS关键词HELPER-CELL DIFFERENTIATION ; E3 UBIQUITIN LIGASES ; NF-KAPPA-B ; DEUBIQUITINATING ENZYMES ; T-CELLS ; INFLAMMATORY RESPONSES ; T(H)2 DIFFERENTIATION ; ITCH ; ACTIVATION ; EXPRESSION
原始文献类型Article
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文献类型期刊论文
条目标识符https://kms.shanghaitech.edu.cn/handle/2MSLDSTB/28683
专题生命科学与技术学院_硕士生
生命科学与技术学院_特聘教授组_钱友存组
通讯作者Qian, Youcun
作者单位
1.Univ Chinese Acad Sci, Chinese Acad Sci,Shanghai Inst Nutr & Hlth, CAS Ctr Excellence Mol Cell Sci,Shanghai Inst Bio, Key Lab Tissue Microenvironm & Tumor, Shanghai, Peoples R China
2.ShanghaiTech Univ, Sch Life Sci & Technol, Shanghai, Peoples R China
通讯作者单位生命科学与技术学院
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Chen, Siyuan,Yun, Fenglin,Yao, Yikun,et al. USP38 critically promotes asthmatic pathogenesis by stabilizing JunB protein[J]. JOURNAL OF EXPERIMENTAL MEDICINE,2018,215(11):2850-2867.
APA Chen, Siyuan.,Yun, Fenglin.,Yao, Yikun.,Cao, Mengtao.,Zhang, Yifan.,...&Qian, Youcun.(2018).USP38 critically promotes asthmatic pathogenesis by stabilizing JunB protein.JOURNAL OF EXPERIMENTAL MEDICINE,215(11),2850-2867.
MLA Chen, Siyuan,et al."USP38 critically promotes asthmatic pathogenesis by stabilizing JunB protein".JOURNAL OF EXPERIMENTAL MEDICINE 215.11(2018):2850-2867.
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