Enhanced TLR-mediated NF-IL6 dependent gene expression by Trib1 deficiency.

ABSTRACT: Toll-like receptors (TLRs) recognize a variety of microbial components and mediate downstream signal transduction pathways that culminate in the activation of nuclear factor kappaB (NF-kappaB) and mitogen-activated protein (MAP) kinases. Trib1 is reportedly involved in the regulation of NF-kappaB and MAP kinases, as well as gene expression in vitro. To clarify the physiological function of Trib1 in TLR-mediated responses, we generated Trib1-deficient mice by gene targeting. Microarray analysis showed that Trib1-deficient macrophages exhibited a dysregulated expression pattern of lipopolysaccharide-inducible genes, whereas TLR-mediated activation of MAP kinases and NF-kappaB was normal. Trib1 was found to associate with NF-IL6 (also known as CCAAT/enhancer-binding protein beta). NF-IL6-defi

SUBMITTER: Yamamoto M 

PROVIDER: S-EPMC2118688 | biostudies-literature | 2007 Sep

REPOSITORIES: biostudies-literature