作者: Meghan E. Pennini , Yi Liu , Jianqi Yang , Colleen M. Croniger , W. Henry Boom
DOI: 10.4049/JIMMUNOL.179.10.6910
关键词: Nuclear protein 、 Biology 、 Binding site 、 Regulation of gene expression 、 Promoter 、 Gene isoform 、 Ccaat-enhancer-binding proteins 、 Molecular biology 、 Chromatin immunoprecipitation 、 CIITA
摘要: TLR2 signaling by Mycobacterium tuberculosis 19-kDa lipoprotein (LpqH) inhibits IFN-γ-induced expression of CIITA macrophages. Microarray analysis, quantitative RT-PCR, and Western blots showed that LpqH induced C/EBPβ C/EBPδ in kinetic correlation with inhibition expression. Of the isoforms, liver inhibitory protein (LIP) was notably liver-activating increased LpqH. Putative C/EBP binding sites were identified promoters I IV (pI pIV). (LIP protein) to biotinylated oligodeoxynucleotide containing pI or pIV sites, chromatin immunoprecipitation endogenous pIV. Constitutive LIP inhibited transfected cells. In summary, C/EBPδ, their pIV, macrophages, suggesting a role for as novel regulator