The Journal of Experimental Medicine
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Published 17 June 2002. doi:10.1084/jem.20020408
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© Rockefeller University Press, 0022-1007/2002/6/1647/ $5.00
The Journal of Experimental Medicine, Volume 195, Number 12, June 17, 2002 1647-1652

Brief Definitive Report

 Protein Kinase C ß Controls Nuclear Factor {kappa}B Activation in B Cells Through Selective Regulation of the I{kappa}B Kinase {alpha}

Kaoru Saijo1, Ingrid Mecklenbräuker1, Angela Santana1, Michael Leitger2, Christian Schmedt1 and Alexander Tarakhovsky1

1 Laboratory of Lymphocyte Signaling, Rockefeller University, New York, NY 10021
2 Max-Plank-Institut für Experimentelle Endokrinologie, Fedor-Lynen-Str. 7, 30625 Hannover, Germany

Address correspondence to Kaoru Saijo or Alexander Tarakhovsky, Laboratory of Lymphocyte Signaling, Rockefeller University, 1230 York Ave., New York, NY 10021. Phone: 212-327-8265 (K. Saijo) or 8256 (A. Tarakhovsky); Fax: 212-327-8258; E-mail: saijok{at}mail.rockefeller.edu or tarakho{at}mail.rockefeller.edu

Activation of the nuclear factor (NF)-{kappa}B transcription complex by signals derived from the surface expressed B cell antigen receptor controls B cell development, survival, and antigenic responses. Activation of NF-{kappa}B is critically dependent on serine phosphorylation of the I{kappa}B protein by the multi-component I{kappa}B kinase (IKK) containing two catalytic subunits (IKK{alpha} and IKKß) and one regulatory subunit (IKK{gamma}). Using mice deficient for protein kinase C ß (PKCß) we show an essential role of PKCß in the phosphorylation of IKK{alpha} and the subsequent activation of NF-{kappa}B in B cells. Defective IKK{alpha} phosphorylation correlates with impaired B cell antigen receptor–mediated induction of the pro-survival protein Bcl-xL. Lack of IKK{alpha} phosphorylation and defective NF-{kappa}B induction in the absence of PKCß explains the similarity in immunodeficiencies caused by PKCß or IKK{alpha} ablation in B cells. Furthermore, the well established functional cooperation between the protein tyrosine kinase Bruton's tyrosine kinase (Btk), which regulates the activity of NF-{kappa}B and PKCß, suggests PKCß as a likely serine/threonine kinase component of the Btk-dependent NF-{kappa}B activating signal transduction chain downstream of the BCR.

Key Words: B cell survival • B cell receptor • signal transduction • I{kappa}B kinase complex • Btk


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