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Am J Physiol Cell Physiol 283: C347-C357, 2002. First published February 27, 2002; doi:10.1152/ajpcell.00166.2001
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Vol. 283, Issue 1, C347-C357, July 2002

Differential requirement for NF-kappa B-inducing kinase in the induction of NF-kappa B by IL-1beta , TNF-alpha , and Fas

Maria P. Russo1, Brydon L. Bennett2, Anthony M. Manning2, David A. Brenner1,3, and Christian Jobin1,3

1 Department of Medicine and Center for Gastrointestinal Biology and Disease and 3 Department of Biochemistry and Biophysics, University of North Carolina, Chapel Hill, North Carolina 27599-7080; and 2 Signal Pharmaceuticals, Inc., San Diego, California 92121

In this study, we examined the role of the nuclear factor-kappa B (NF-kappa B)-inducing kinase (NIK) in distinct signaling pathways leading to NF-kappa B activation. We show that a dominant-negative form of NIK (dnNIK) delivered by adenoviral (Ad5dnNIK) vector inhibits Fas-induced Ikappa Balpha phosphorylation and NF-kappa B-dependent gene expression in HT-29 and HeLa cells. Interleukin (IL)-1beta - and tumor necrosis factor-alpha (TNF-alpha )-induced NF-kappa B activation and kappa B-dependent gene expression are inhibited in HeLa cells but not in Ad5dnNIK-infected HT-29 cells. Moreover, Ad5dnNIK failed to sensitize HT-29 cells to TNF-alpha -induced apoptosis at an early time point. However, cytokine- and Fas-induced signals to NF-kappa B are finally integrated by the Ikappa B kinase (IKK) complex, since Ikappa Balpha phosphorylation, NF-kappa B DNA binding activity, and IL-8 gene expression were strongly inhibited in HT-29 and HeLa cells overexpressing dominant-negative IKKbeta (Ad5dnIKKbeta ). Our findings support the concept that cytokine signaling to NF-kappa B is redundant at the level of NIK. In addition, this study demonstrates for the first time the critical role of NIK and IKKbeta in Fas-induced NF-kappa B signaling cascade.

interleukin-8; inflammation; intestinal epithelial cells; signal transduction


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