Activation by IKKα of a Second, Evolutionary Conserved, NF-κB Signaling Pathway

Author:

Senftleben Uwe12,Cao Yixue1,Xiao Gutian3,Greten Florian R.1,Krähn Gertraud14,Bonizzi Giuseppina1,Chen Yi1,Hu Yinling1,Fong Abraham3,Sun Shao-Cong3,Karin Michael1

Affiliation:

1. Laboratory of Gene Regulation and Signal Transduction, Department of Pharmacology, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA.

2. Clinic for Anesthesiology, University of Ulm, Steinhövelstrasse 9, 89075 Ulm, Germany.

3. Department of Microbiology and Immunology, Pennsylvania State University College of Medicine, Hershey, PA 17033, USA.

4. Department of Dermatology, University of Ulm, Oberer Eselsberg 40, 89081 Ulm, Germany.

Abstract

In mammals, the canonical nuclear factor κB (NF-κB) signaling pathway activated in response to infections is based on degradation of IκB inhibitors. This pathway depends on the IκB kinase (IKK), which contains two catalytic subunits, IKKα and IKKβ. IKKβ is essential for inducible IκB phosphorylation and degradation, whereas IKKα is not. Here we show that IKKα is required for B cell maturation, formation of secondary lymphoid organs, increased expression of certain NF-κB target genes, and processing of the NF-κB2 (p100) precursor. IKKα preferentially phosphorylates NF-κB2, and this activity requires its phosphorylation by upstream kinases, one of which may be NF-κB–inducing kinase (NIK). IKKα is therefore a pivotal component of a second NF-κB activation pathway based on regulated NF-κB2 processing rather than IκB degradation.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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