Functional characterization of the NF-kB binding site in the human NOD2 promoter

作     者：Chaofeng Hu Liping Sun Yiling Hu Daxiang Lu Huadong Wang Suisheng Tang 

作者机构：Department of PathophysiologyMedical CollegeJinan UniversityGuangzhouChina Department of Physiology and BiophysicsFaculty of MedicineDalhousie UniversityHalifaxNSCanada Data Mining DepartmentInstitute for Infocomm ResearchSingapore 

出 版 物：《Cellular & Molecular Immunology》 (中国免疫学杂志（英文版）)

年 卷 期：2010年第7卷第4期

页      面：288-295页

核心收录：

学科分类：083002[工学-环境工程] 0830[工学-环境科学与工程（可授工学、理学、农学学位）] 08[工学] 

基　　金：supported by grants from the Natural Science Foundation of Guangdong Province(No.06025159) the Natural Science Foundation from Department of Education of Guangdong Province(No.126(2005)) 

主　　题：innate immunity NF-kB binding site NOD2 promoter 

摘      要：Nucleotide-binding and oligomerization domain 2(NOD2),a member of the NOD protein family,plays an important role in innate *** response to pathogen attack,NOD2 stimulates cytokine and defensin production by activating nuclear factor(NF)-kB,a key transcription factor responsible for mediating downstream ***,the mechanism linking NOD2 regulation and NF-kB activation is poorly *** bioinformatics,we found a completely preserved canonical NF-kB binding site in the NOD2 core promoter(216 to 225 bp)in both humans and *** functional role of this NF-kB binding site was investigated using the enhanced green fluorescent protein(EGFP)reporter system,site-directed mutagenesis,the NF-kB activation inhibitor(JSH-23)and the chromatin immunoprecipitation(ChIP)*** results show that the NF-kB binding site is critical for regulation of the NOD2 *** deletion of the NF-kB binding elements within the NOD2 promoter or treatment with an NF-kB activation inhibitor could lead to a significant loss of NOD2 promoter activity as detected by reporter gene *** canonical NF-kB binding site was bound by NF-kB as determined by the ChIP *** on these results,we suggest a positive feedback regulation between NF-kB and NOD2,which may represent an efficient mechanism in response to pathogen invasion.