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| 1 | Regulation of Toll-like receptor signaling in innate immunity显示文摘Toll-like receptors sense invading pathogens by recognizing a wide variety of conserved pathogen-associated molecular patterns(PAMPs).The members of the TLR family selectively utilize adaptor proteins MyD88,TRIF,TIRAP and TRAM to activate overlapping but distinct signal transduction pathways which trigger production of different panels of mediators such as proinflammatory cytokines and type I interferon.These mediators not only control innate immunity but also direct subsequently developed adaptive immunity.TLR activation is strictly and finely regulated at multiple levels of the signal transduction pathways. | AN HuaZhang,QIAN Cheng & CAO XueTao National Key Laboratory of Medical Immunology & Institute of Immunology,Second Military Medical University,Shanghai 200433,China | 2010 | Science China(Life Sciences)2010，53，1： | 29 |
| 2 | TAOK1 negatively regulates IL-17-mediated signaling and inflammation显示文摘Interleukin 17(IL-17)is an important cytokine that can induce tissue inflammation and is involved in the pathogenesis of numerous autoimmune diseases.However,the regulation of its signaling transduction has not been well described.In this study,we report that thousand and one kinase 1(TAOK1)functions as a negative regulator of IL-17-mediated signal transduction and inflammation.TAOK1 knockdown promotes IL-17-induced cytokine and chemokine expression and the activation of mitogen-activated protein kinases and nuclear factor-κB.We further demonstrate that TAOK1 interacts with IL-17 receptor A(IL-17RA)independent of its kinase activity,and TAOK1 dose-dependently prevents the formation of the IL-17R-Act1(nuclear factor activator 1,also known as tumor necrosis factor receptor-associated factor 3 interacting protein 2)complex.Consistent with this,TAOK1 deficiency exacerbates colitis in the 2,4,6-trinitrobenzenesulfonic acid-induced experimental model of inflammatory bowel disease,likely by its promotion of the IL-17-mediated signaling pathway.TAOK1 expression is decreased in the colons of ulcerative colitis patients.In conclusion,these findings suggest that TAOK1 is involved in the development of IL-17-related autoimmune disorders. | Zhaoru Zhang Zhen Tang Xianwei Ma Kai Sun Liping Fan Jie Fang Jianping Pan Xiaojian Wang Huazhang An Jun Zhou | 2018 | Cellular & Molecular Immunology2018，15，8： | 10 |
| 3 | MEF2C promotes M1 macrophage polarization and Th1 responses显示文摘The polarization of macrophages to the M1 or M2 phenotype has a pivotal role in inflammation and host defense;however,the underlying molecular mechanism remains unclear.Here,we show that myocyte enhancer factor 2 C(MEF2C)is essential for regulating M1 macrophage polarization in response to infection and inflammation.Global gene expression analysis demonstrated that MEF2C deficiency in macrophages downregulated the expression of M1 phenotypic markers and upregulated the expression of M2 phenotypic markers.MEF2C significantly promoted the expression of interleukin-12 p35 subunit(Il12a)and interleukin-12 p40 subunit(Il12b).Myeloid-specific Mef2c-knockout mice showed reduced IL-12 production and impaired Th1 responses,which led to susceptibility to Listeria monocytogenes infection and protected against DSS-induced IBD in vivo.Mechanistically,we showed that MEF2C directly activated the transcription of Il12a and Il12b.These findings reveal a new function of MEF2C in macrophage polarization and Th1 responses and identify MEF2C as a potential target for therapeutic intervention in inflammatory and autoimmune diseases. | Xibao Zhao Qianqian Di Han Liu Jiazheng Quan Jing Ling Zizhao Zhao Yue Xiao Han Wu Zherui Wu Wengang Song Huazhang An Weilin Chen | 2022 | Cellular & Molecular Immunology2022，19，4： | 4 |
| 4 | Involvement of ERK, p38 and NF-kB signal transduction in regulation of TLR2, TLR4 and TLR9 gene expression induced by lipopolysaccha- ride in mouse dendritic cells显示文摘 | HUAZHANG AN YIZHI YU | 2002 | Immunology2002，，106： | 1 |
| 5 | The primers are referenced to Involvement of ERK,p38 and NF-KB singal transduction in regulation of TLR2,TLR4 and TLR9 gene expression induced by lipopolysaccharide in mouse dendritic cell显示文摘 | Huazhang AN Golen DT Wang JE | 2002 | Immunology2002，106，： | 1 |
| 6 | Differentially expressed gene profiles between multidrug resistant gastric adenocarcinoma cells and their parental cells显示文摘 | Yanqiu Zhao Han You Fei Liu Huazhang An Yongquan Shi Qiang Yu Daiming Fan | 2002 | Cancer Letters2002，，2： | 1 |
| 7 | SHP-2 Phosphatase Negatively Regulates the TRIF Adaptor Protein-Dependent Type I Interferon and Proinflammatory Cytokine Production显示文摘 | Huazhang An Wei Zhao Jin Hou Yan Zhang Yun Xie Yuejuan Zheng Hongmei Xu Cheng Qian Jun Zhou Yizhi Yu Shuxun Liu Gensheng Feng Xuetao Cao | 2006 | Immunity2006，，6： | 1 |
| 8 | Correction to: TAOK1 negatively regulates IL-17-mediated signaling and inflammation显示文摘Correction to:Cellular&Molecular Immunology(2018).http://gffzzd3cc09b8251d45dfsw9bx5fbnkxck6f5q.ffgz.tsg.suse.edu.cn/10.1038/cmi.2017.158;published online 5 February 2018 In this article,published online 5 February 2018,the second primer of mouse actin,il-6,il-1β,TNFα,cxcl1,cxcl2 and ccl20 in Table 2 should be marked as“reverse primer”instead of“forward primer”.Corrected Table 2 is shown below.The authors regret the errors. | Zhaoru Zhang Zhen Tang Xianwei Ma Kai Sun Liping Fan Jie Fang Jianping Pan Xiaojian Wang Huazhang An Jun Zhou | 2018 | Cellular & Molecular Immunology2018，15，10： | 0 |
| 9 | Cloning and Characterization of DULP,a Novel Ubiquitin-Like Molecule from Human Dendritic Cells显示文摘We identified a novel ubiquitin-like molecule DULP from human dendritic cells. DULP contains a domain that shares 26% identity and 34% similarity with ubiquitin,and it possesses the corresponding Ile-44 hydrophobic patch used by mono-or poly-ubiquitin to interact with a ubiquitin-interaction motif(UIM) or ubiquitin-associated domain(UBA) . Lysine residue corresponding to 6 of ubiquitin,which is involved in the formation of a multi-ubiquitin chain that can bind proteasomal subunit Rpn10/S5a,is also conserved in its ubiquitin-homology domain. However,DULP does not possess the highly conserved C-terminus Gly-Gly required for ubiquitin conjugation or the Lys-48 required for the formation of polyubiquitin chain to target substrates for degradation,suggesting it might be a novel ubiquitin-domain protein(UDP) . DULP was found widely expressed in many cells and the ubiquitin-homology domain was not cleaved. We also confirmed that DULP expression was enriched in the nucleus and much weaker in the cytosol. Besides,we found that overexpression of DULP in 293T cells induced apoptosis,which might not be associated with the mitochondrial or proteasome pathway,with the specific mechanism remain unclear. Further investigations are needed to identify the precise biological functions of DULP. | Guoyan Liu Shuxun Liu Ping Li Ling Tang Yanmei Han Huazhang An Jiangyan Li Xiankun Dai Nan Li Xuetao Cao Yizhi Yu | 2009 | Cellular & Molecular Immunology2009，6，1： | 0 |
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