Abstract
The NF-kB family consists of a group of inducible transcription factors which regulate immune and inflammatory responses and protect cells from undergoing apoptosis in response to cellular stress. A number of signal transduction cascades can activate the NF-kB pathway to result in the translocation of the NF-kB proteins from the cytoplasm to the nucleus where they activate the expression of specific cellular genes. In this review, we discuss cellular genes which are regulated by NF-kB and disease states which are associated with constitutive activation of the NF-kB pathway. Strategies to prevent prolonged activation of the NF-kB pathway are also discussed.
Keywords: NF-kB, Pathogenesis, apoptosis, NF-kB proteins, including interleukin 1b (IL-1b), tumor necrosis factor(TNFa), nitric oxide synthase(iNOS), oxide (NO), cyclo-oxygenase (COX-2), (cIAP1, cIAP2, IXAP)
Current Molecular Medicine
Title: Role of the NF-kB Pathway in the Pathogenesis of Human Disease States
Volume: 1 Issue: 3
Author(s): Yumi Yamamoto and Richard B. Gaynor
Affiliation:
Keywords: NF-kB, Pathogenesis, apoptosis, NF-kB proteins, including interleukin 1b (IL-1b), tumor necrosis factor(TNFa), nitric oxide synthase(iNOS), oxide (NO), cyclo-oxygenase (COX-2), (cIAP1, cIAP2, IXAP)
Abstract: The NF-kB family consists of a group of inducible transcription factors which regulate immune and inflammatory responses and protect cells from undergoing apoptosis in response to cellular stress. A number of signal transduction cascades can activate the NF-kB pathway to result in the translocation of the NF-kB proteins from the cytoplasm to the nucleus where they activate the expression of specific cellular genes. In this review, we discuss cellular genes which are regulated by NF-kB and disease states which are associated with constitutive activation of the NF-kB pathway. Strategies to prevent prolonged activation of the NF-kB pathway are also discussed.
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Cite this article as:
Yamamoto Yumi and Gaynor B. Richard, Role of the NF-kB Pathway in the Pathogenesis of Human Disease States, Current Molecular Medicine 2001; 1 (3) . https://dx.doi.org/10.2174/1566524013363816
DOI https://dx.doi.org/10.2174/1566524013363816 |
Print ISSN 1566-5240 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5666 |
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