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TLR4基因结构和功能的生物信息学分析 被引量:1

Bioinformatics Analysis of Structure and Function of TLR4 Gene
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摘要 目的运用生物信息学的各种方法,对TLR4基因的结构和功能进行深入分析。方法依托生物信息学的各种软件,对TLR4基因启动子及其所编码的氨基酸理化性质、信号肽、跨膜结构、蛋白质的二级结构、蛋白质三级结构、蛋白质翻译后修饰、蛋白质相互作用进行生物信息学分析。结果 TLR4基因只有一个启动子;TLR4蛋白属于亲水的不稳定蛋白,等电点为5.88;TLR4蛋白大多数位于膜外的分泌蛋白并且有信号肽;二级结构以α螺旋和无规则卷曲为主;三级结构稳定可靠;N-糖基化位点和O-糖基化位点各有10和4位;磷酸化的位点有Ser:21,Thr:6,Tyr:7;TLR4蛋白可以与10个蛋白发生作用。结论深入分析TLR4基因的结构和功能,研究其与肝脏疾病之间的关系有很大的意义。 Objective To analyze the structure and function of TLR4 gene by bioinformatics.Methods Based on various bioinformatics software,the TLR4 gene promoter and its encoded amino acid physicochemical properties,signal peptide,transmembrane structure,protein secondary structure,protein tertiary structure and protein post-translational modification were studied.Protein interactions were analyzed by bioinformatics.Results There was only one promoter of the TILR4 gene,which was a hydrophilic unstable protein.The isoelectric point of 5.88 TLR4 protein was mainly located in the secretory protein with signal peptide,and the secondary structure was mainlyαhelix and irregular curl.There were 10 and 4 sites in the third order structure,10 and 4 sites respectively in the n-and o-glycosylation sites,and the phosphorylated sites were Ser:21,Thr:6,Tyr:7 TLR4 proteins,which can interact with 10 proteins.Conclusion It is of great significance to analyze the structure and function of TLR4 gene and study its relationship with liver diseases.
作者 郑洋 王佳慧 梁天坚 汪磊 赵铁建 ZHENG Yang;WANG Jiahui;LIANG Tianjian;WANG Lei;ZHAO Tiejian(Department of Medicine,Faculty of Cinese Medicine Science Guangxi University of Chinese Medicine,Nanning 530021,Guangxi,China;Basic Medical School of Guangxi University of Chinese Medicine,Nanning 530021,Guangxi,China)
出处 《中华中医药学刊》 CAS 北大核心 2020年第1期157-160,I0028,I0029,共6页 Chinese Archives of Traditional Chinese Medicine
基金 国家自然科学基金(81460682,81660705) 广西中医药大学研究生重点创新项目(YCSZ2018013,YCSY2018004)。
关键词 TLR4 结构 功能 生物信息学 TLR4 structure function bioinformatics
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  • 1Friedman SL. Mechanisms of hepatic fibrogenesis[ J ]. Gastroenter- ology, 2008, 134 (6) : 1655-1669.
  • 2Shibata T, Motoi Y, Tanimura N, Yamakawa N, Akashi-TakamuraS, Miyake K. Intracellular TLR4lMD-2 in macrophages senses Gram-negative bacteria and induces a unique set of LPS-dependent genes[J]. Int Immunol , 2011,23(8)=503-510.
  • 3Seki E, De Minicis S, Osterreicher CH, Kluwe J, Osawa Y, Bren- ner DA, et al. TLR4 enhances TGF-beta signaling and hepatic fi- brosis [J].Nat Med, 2007, 13 ( 11 ) : 1324-1332.
  • 4Hua J, Qiu de K, Li JQ, Li EL, Chen XY, Peng YS. Expression of Toll-like receptor 4 in rat liver during the course of carbon tetrachlo- ride-induced liver injury [ J ]. J Gastroenterol Hepatol, 2007, 22 (6) : 862-869.
  • 5Isayarna F, Hines IN, Kremer M, Milton R J, Byrd CL, Perry AW, et al. LPS signaling enhances hepatic fibrogenesis caused by experirnen- tal cholestasis in mice [ J ]. Am J Physiol Gastrointest Liver Physiol, 2006, 290(6) :G1318-G1328,.
  • 6Steib CJ, Hartmann AC, v Hesler C, Benesic A, Hennenberg M, Bilz- er M, et al. Intraperitoneal LPS amplifies portal hypertension in rat liver fibrosis[J]. Lab Invest, 2010, 90(7) :1024-1032.
  • 7Guo J, Friedman SL. Toll-like receptor 4 signaling in liver injury and hepatic fibrogenesis[J]. Fibrogenesis Tissue Repair, 2010, 3:21.
  • 8Su GL, Klein RD, Aminlari A, Zhang HY, Steinstraesser L, Alarc~ WH, et al. Kupffer cell activation by lipopolysaccharide in rats= roI for lipopolysaccharide binding protein and toll-like receptor 4 [ J] Hepatology, 2000, 31 (4) :932-936.
  • 9Chen LC, Gordon RE, Laskin JD, Laskin DL. Role of TLR-4 in liv- er maerophage and endothelial cell responsiveness dudng acute en- dotoxemia[J]. Exp Mol Pathol, 2007, 83(3) :311-326.
  • 10Chen LC, Laskin JO, Gordon MK, LaskJn DL. Regulation of TREM ex- pression in hepatic macrophages and endothelial cells during acute en- dotoxemia[J]. Fxp Mol Pathol, 2008, 84(2) :145-155.

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