國家衛生研究院 NHRI:Item 3990099045/6002
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    jsp.display-item.identifier=請使用永久網址來引用或連結此文件: http://ir.nhri.org.tw/handle/3990099045/6002


    题名: The kinase GLK controls autoimmunity and NF-kappa B signaling by activating the kinase PKC-theta in T cells
    其它题名: The kinase GLK controls autoimmunity and NF-κB signaling by activating the kinase PKC-θ in T cells
    作者: Chuang, HC;Lan, JL;Chen, DY;Yang, CY;Chen, YM;Li, JP;Huang, CY;Liu, PE;Wang, X;Tan, TH
    贡献者: Immunology Research Center
    摘要: Protein kinase C-theta (PKC-theta) is required for activation of the transcription factor NF-kappa B induced by signaling via the T cell antigen receptor (TCR); however, the direct activator of PKC-theta is unknown. We report that the kinase GLK (MAP4K3) directly activated PKC-theta during TCR signaling. TCR signaling activated GLK by inducing its direct interaction with the upstream adaptor SLP-76. GLK-deficient mice had impaired immune responses and were resistant to experimental autoimmune encephalomyelitis. Consistent with that, people with systemic lupus erythematosus had considerable enhanced GLK expression and activation of PKC-theta and the kinase IKK in T cells, and the frequency of GLK-overexpressing T cells was directly correlated with disease severity. Thus, GLK is a direct activator of PKC-theta, and activation of GLK-PKC-theta-IKK could be used as new diagnostic biomarkers and therapeutic targets for systemic lupus erythematosus
    日期: 2011-10
    關聯: Nature Immunology. 2011 Oct;12(11):1113-1118.
    Link to: http://dx.doi.org/10.1038/ni.2121
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=1529-2908&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000296500100017
    Cited Times(Scopus): http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=80054953932
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