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NF‐κB Signaling
Author(s) -
EGAN LAURENCE J.,
TORUNER MURAT
Publication year - 2006
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1196/annals.1326.009
Subject(s) - transcription factor , nf κb , inflammation , signal transduction , regulator , apoptosis , nfkb1 , biology , programmed cell death , cancer research , microbiology and biotechnology , inflammatory bowel disease , disease , immunology , gene , genetics , medicine
The transcription factor, nuclear factor‐κB (NF‐κB), is a dominant regulator of the expression of hundreds of genes, many of which play important roles in the regulation of inflammation and programmed cell death (apoptosis). Since the discovery of NF‐κB in the mid 1980s, this transcription factor has been the subject of intense investigation. Excess or inappropriate activation of NF‐κB has been observed in human inflammatory bowel disease and in a host of other inflammatory diseases and type of cancer. Functional studies in animals have shed light on the role of NF‐κB in broader pathophysiological contexts. From such studies, it has become quite clear that NF‐κB plays unique and distinct functions in different cell types. Because of the importance of NF‐κB in signaling inflammation, and in inhibiting programmed cell death, many pharmaceutical companies are developing small‐molecule inhibitors of this pathway. In this article, we evaluate the relative pros and cons of blocking NF‐κB as a therapeutic approach for inflammatory bowel disease. On the basis of the results of studies in animals that have primarily used genetic approaches to inhibit NF‐κB activity, we suggest that there are certain niche indications for blocking NF‐κB in inflammatory bowel disease that offer particular promise.