NF-κB signaling pathway in the treatment of the role of inflammatory enteritis_0.doc

 PAGE \* MERGEFORMAT 13 NF-κB signaling pathway in the treatment of the role of inflammatory enteritis [Abstract] discusses the NF-κB signal transduction pathway related protein structures, pathways and activation of different targets based on NF-κB blockade in the treatment of IBD in the future for the study of NF-κB in the pathogenesis of IBD to provide documentary evidence to support the mechanism . [Keywords:] NF-κB; inflammatory enteritis Inflammatory colitis (Inflammatory bowel disease, IBD) is not yet fully understood etiology and pathology of chronic inflammation associated with autoimmune diseases. Is generally believed that the incidence of IBD in susceptible genes, such as the IBD5, IL23R and other changes in circumstances, environmental factors and intestinal flora, food antigens hapten cause intestinal barrier dysfunction, excessive intestinal mucosal immune response and inflammatory reaction occurs. IBD and the relationship between NF κB has drawn people’s attention, the relationship between the channel and also the recent IBD a hot research field. 1 NF κB signaling pathway Introduction 1.1 NF κBRel family of NF-κBRel family, including p100, p105, p52, p65/RelA, c-Rel and other. NF-κB heterodimer formation of homo-and post-κB target gene locus 5’-GGGACTTTCC-3 ‘combination. each family member contains an N-terminal 300 amino acids by the so-called Rel homology domain (rel homology domain, RHD), a highly conserved region of the structure contain DNA binding sites, NF -κB / Rel proteins that dimerization domain, and the κB binding site, nuclear localization sequence (nuclear localization sequence, NLS). usually refers to the p65/p50 NF-κB is a dimer, that relA protein transcription factor, is a multi-directional transcription factor, both are constitutively nuclear transcription factor (consititutive nuclear transcription factor), also belong to the nuclear transcription factor inducible (inducible nuclear transcription factor), can re