reply: Kinase regulation in inflammatory response

Osman Nidai Ozes, Lindsey D. Mayo, Jason A. Gustin, Susan R. Pfeffer, Lawrence M. Pfeffer and David B. Donner
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Osman Nidai Ozes: Department of Microbiology and Immunology Indiana University School of Medicine and the Walther Oncology Center
Lindsey D. Mayo: Department of Microbiology and Immunology Indiana University School of Medicine and the Walther Oncology Center
Jason A. Gustin: Department of Microbiology and Immunology Indiana University School of Medicine and the Walther Oncology Center
Susan R. Pfeffer: University of Tennessee Health Science Center
Lawrence M. Pfeffer: University of Tennessee Health Science Center
David B. Donner: Department of Microbiology and Immunology Indiana University School of Medicine and the Walther Oncology Center

Nature, 2000, vol. 406, issue 6794, 368-368

Abstract: Abstract Ozes et al . reply Delhase et al. take issue with our claim1 that Akt induces activation of NF-κB by phosphorylating IKKα, contending that IKKα plays no role in the activation by TNF of NF-κB, and consequently that Akt could not affect NF-κB through IKKα. They point out that Hu et al.2 have shown that cells deficient in IKKα have normal TNF-induced NF-κB activity, but this has been refuted by Li et al.3, who reported significant reduction of TNF-induced NF-κB in IKKα-deficient cells. Indeed, the observations of Hu et al.2 show that degradation of IκBα is diminished in cells from IKKα-deficient mice and are therefore not consistent with the conclusion that IKKα plays no role in TNF induction of NF-κB. Furthermore, deficiency of IKKβ only partially impairs TNF-induced NF-κB activation4,5, which reserves a role for IKKα in this pathway. Others5,6,7 have shown that activation of the IKK complex is dependent on the kinase activity of IKKα to activate IKKβ. Thus, strong evidence supports a role for IKKα in TNF induction of NF-κB.

Date: 2000
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DOI: 10.1038/35019157

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