Nf-kappab Signaling: Pros and Cons of Altering Nf-kappab As a Therapeutic Approach.
From: Clinical Science Institute, University College Hospital, Galway, Ireland. laurence.egan@nuigalway.ie
Annals of the New York Academy of Sciences
- Publish Date: Aug 2006
- ISSN: 0077-8923
- Volume: 1072
- Issue:
- Pages: 114-22
- Medium: Print
- Language: English
- Citation (JAMA): Egan Laurence J, Toruner Murat, et al. Nf-kappab Signaling: Pros and Cons of Altering Nf-kappab As a Therapeutic Approach.. Ann. N. Y. Acad. Sci. Aug 2006;1072:114-22
Abstract
The transcription factor, nuclear factor-kappaB (NF-kappaB), 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-kappaB in the mid 1980s, this transcription factor has been the subject of intense investigation. Excess or inappropriate activation of NF-kappaB 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-kappaB in broader pathophysiological contexts. From such studies, it has become quite clear that NF-kappaB plays unique and distinct functions in different cell types. Because of the importance of NF-kappaB 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-kappaB 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-kappaB activity, we suggest that there are certain niche indications for blocking NF-kappaB in inflammatory bowel disease that offer particular promise.
Mesh Headings (Keywords): Animals, Disease Models, Animal, Humans, Inflammatory Bowel Diseases, Mice, NF-kappa B, Signal Transduction
Check for Full Text / PubMed Unique Identifier (PMID): 17057194
This abstract is part of PubMed, a service of the U.S. National Library of Medicine. PubMed includes more than 17 million citations from MEDLINE and other life science journals for biomedical articles. See Copyright and Disclaimers.
Linked medical terms appearing on this page are added by Healia to help readers find more information and are not part of the original PubMed document.
The data herein was last updated on July 8th, 2008 and may not reflect the most current and accurate data available from NLM.