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IL-17 induced NOTCH1 activation in oligodendrocyte progenitor cells enhances proliferation and inflammatory gene expression

文献类型：期刊论文

作者Wang, Chenhui1,2,13; Zhang, Cun-Jin1; Martin, Bradley N.1; Bulek, Katarzyna1; Kang, Zizhen1; Zhao, Junjie1; Bian, Guanglin1; Li, Xiaoxia1; Zhang, Cun-Jin3; Martin, Bradley N.4
刊名NATURE COMMUNICATIONS
出版日期2017
卷号8期号:-页码:15508
关键词Genetics Issue 122 artificial RNA binding factors protein engineering splicing factors alternative splicing PUF scaffold RNA binding proteins cancer
ISSN号2041-1723
DOI10.1038/ncomms15508
文献子类Article
英文摘要NOTCH1 signalling contributes to defective remyelination by impairing differentiation of oligodendrocyte progenitor cells (OPCs). Here we report that IL-17 stimulation induces NOTCH1 activation in OPCs, contributing to Th17-mediated demyelinating disease. Mechanistically, IL-17R interacts with NOTCH1 via the extracellular domain, which facilitates the cleavage of NOTHC1 intracellular domain (NICD1). IL-17-induced NOTCH1 activation results in the interaction of IL-17R adaptor Act1 with NICD1, followed by the translocation of the Act1-NICD1 complex into the nucleus. Act1-NICD1 are recruited to the promoters of several NOTCH1 target genes (including STEAP4, a metalloreductase important for inflammation and cell proliferation) that are specifically induced in the spinal cord by Th17 cells. A decoy peptide disrupting the IL-17RA-NOTCH1 interaction inhibits IL-17-induced NOTCH1 activation and attenuates Th17-mediated experimental autoimmune encephalitis (EAE). Taken together, these findings demonstrate critical crosstalk between the IL-17 and NOTCH1 pathway, regulating Th17-induced inflammatory and proliferative genes to promote demyelinating disease.
学科主题Science & Technology - Other Topics
WOS关键词EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS ; CENTRAL-NERVOUS-SYSTEM ; T-HELPER TYPE-1 ; MULTIPLE-SCLEROSIS ; UBIQUITIN LIGASE ; ACT1 ; CYTOKINE ; PATHWAY ; T(H)17 ; PATHOGENESIS
语种英语
WOS记录号WOS:000402390000001
出版者NATURE PUBLISHING GROUP
版本出版稿
源URL[http://202.127.25.144/handle/331004/965]  
专题中国科学院上海生命科学研究院营养科学研究所
作者单位1.Cleveland Clin Fdn, Lerner Res Inst, Dept Immunol, Cleveland, OH 44195 USA;
2.Wuhan Inst Biotechnol, Wuhan 430075, Peoples R China;
3.Tianjin Med Univ Gen Hosp, Tianjin Neurol Inst, Dept Neurol & Immunol, Tianjin 300052, Peoples R China;
4.Case Western Reserve Univ, Sch Med, Dept Pathol, Cleveland, OH USA;
5.Shanghai Jiao Tong Univ, Shanghai Inst Immunol, Sch Med, 280 South Chongqing Rd, Shanghai 200025, Peoples R China;
6.Bristol Myers Squibb, Discovery Biol, Princeton, NJ 08540 USA;
7.Binzhou Med Univ Hosp Binzhou City, Dept Endocrinol & Metab, Binzhou City 256603, Shandong, Peoples R China;
8.Northwestern Univ, Feinberg Sch Med, Dept Microbiol Immunol, Chicago, IL 60611 USA;
9.Chinese Acad Sci, Inst Hlth Sci, Shanghai Inst Biol Sci, Shanghai Jiao Tong Univ,Sch Med,Key Lab Stem Cell, Shanghai 200031, Peoples R China;
10.Shanghai Jiao Tong Univ, Shanghai Inst Rheumatol, Shanghai Renji Hosp, Sch Med, Shanghai 200001, Peoples R China;
推荐引用方式
GB/T 7714		 Wang, Chenhui,Zhang, Cun-Jin,Martin, Bradley N.,et al. IL-17 induced NOTCH1 activation in oligodendrocyte progenitor cells enhances proliferation and inflammatory gene expression[J]. NATURE COMMUNICATIONS,2017,8(-):15508.
APA Wang, Chenhui.,Zhang, Cun-Jin.,Martin, Bradley N..,Bulek, Katarzyna.,Kang, Zizhen.,...&,.(2017).IL-17 induced NOTCH1 activation in oligodendrocyte progenitor cells enhances proliferation and inflammatory gene expression.NATURE COMMUNICATIONS,8(-),15508.
MLA Wang, Chenhui,et al."IL-17 induced NOTCH1 activation in oligodendrocyte progenitor cells enhances proliferation and inflammatory gene expression".NATURE COMMUNICATIONS 8.-(2017):15508.

入库方式： OAI收割

来源：上海营养与健康研究所

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