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Articles in PresS, published online ahead of print February 27, 2002
Am J Physiol Cell Physiol, 10.1152/ajpcell.00166.2001
Submitted on April 2, 2001
Accepted on February 21, 2002
B-inducing kinase (NIK) in the induction of NF-B by IL-1ß, TNF
and Fas
1 Medicine, University of North Carolina, Chapel Hill, NC, USA
2 Signal Pharmaceuticals, San Diego, CA, USA
* To whom correspondence should be addressed. E-mail: job{at}med.unc.edu.
In this study, we examined the role of the NF-B inducing Kinase (NIK) in distinct signaling pathways leading to NF-B activation. We show that a dominant negative form of NIK (dnNIK) delivered by adenoviral (Ad5dnNIK) vector inhibits Fas-induced IB phosphorylation and NF-B-dependent gene expression in HT-29 and Hela cells. IL-1ß and TNF-induced NF-B activation and B-dependent gene expression is inhibited in Hela but not in Ad5dnNIK-infected HT-29 cells. Moreover, Ad5dnNIK failed to sensitized HT-29 cells to TNF-induced apoptosis at an early time point. However cytokines- and Fas-induced signals to NF-B are finally integrated by the IB kinase complex (IKK) since IB phosphorylation, NF-B DNA binding activity and IL-8 gene expression were strongly inhibited in HT-29 and Hela cells overexpressing dominant negative IKKß (Ad5dnIKKß). Our findings support the concept that cytokine signaling to NF-B is redundant at the level of NIK. In addition, this study demonstrates for the first time the critical role of NIK and IKKß in Fas-induced NF-B signaling cascade.
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