國家衛生研究院 NHRI:Item 3990099045/12878
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    NHRI > Immunology Research Center > Tse-Hua Tan > Periodical Articles >  Item 3990099045/12878


    Please use this identifier to cite or link to this item: http://ir.nhri.org.tw/handle/3990099045/12878


    Title: DUSP11 attenuates lipopolysaccharide-induced macrophage activation by targeting TAK1
    Authors: Yang, CY;Chuang, HC;Tsai, CY;Xiao, YZ;Yang, JY;Huang, RH;Shih, YC;Tan, TH
    Contributors: Immunology Research Center
    Abstract: Dual-specificity phosphatase 11 (DUSP11, also named as PIR1) is a member of the atypical DUSP protein tyrosine phosphatase family. DUSP11 is only known to be an RNA phosphatase that regulates noncoding RNA stability. To date, the role of DUSP11 in immune cell signaling and immune responses remains unknown. In this study, we generated and characterized the immune cell functions of DUSP11-deficient mice. We identified TGF-β-activated kinase 1 (TAK1) as a DUSP11-targeted protein. DUSP11 interacted directly with TAK1, and the DUSP11-TAK1 interaction was enhanced by LPS stimulation in bone marrow-derived macrophages. DUSP11 deficiency enhanced the LPS-induced TAK1 phosphorylation and cytokine production in bone marrow-derived macrophages. Furthermore, DUSP11-deficient mice were more susceptible to LPS-induced endotoxic shock. The LPS-induced serum levels of IL-1β, TNF-α, and IL-6 were significantly elevated in DUSP11-deficient mice compared with those of wild-type mice. The data indicate that DUSP11 inhibits LPS-induced macrophage activation by targeting TAK1.
    Date: 2020-08-12
    Relation: Journal of Immunology. 2020 Aug 12;205(6):1644-1652.
    Link to: http://dx.doi.org/10.4049/jimmunol.2000334
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=0022-1767&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000567623300017
    Cited Times(Scopus): https://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85090613917
    Appears in Collections:[Tse-Hua Tan] Periodical Articles
    [Huai-Chia Chuang] Periodical Articles

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