HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Cariappa, A. Articles by Pillai, S. Search for Related Content PubMed PubMed Citation Articles by Cariappa, A. Articles by Pillai, S. Pubmed/NCBI databases Gene GEO Profiles HomoloGene Protein UniGene Substance via MeSH

A Catalytically Inactive Form of Protein Kinase C-Associated Kinase/Receptor Interacting Protein 4, a Protein Kinase C-Associated Kinase That Mediates NF-B Activation, Interferes with Early B Cell Development¹

Massachusetts General Hospital Cancer Center, Harvard Medical School, Boston, MA 02129

Protein kinase C-associated kinase (PKK)/receptor interacting protein 4 (RIP4) is a protein kinase C (PKC) -associated kinase that links PKC to NF-B activation. The kinase domain of PKK is similar to that of RIP, RIP2, and RIP3. We show in this study that PKK is expressed early during lymphocyte development and can be detected in common lymphoid progenitor cells. Targeting of a catalytically inactive version of PKK to lymphoid cells resulted in a marked impairment in pro-B cell generation in the bone marrow. Although peripheral B cell numbers were markedly reduced, differentiation into follicular and marginal zone B cells was not defective in these mice. B-1a and B-1b B cells could not be detected in these mice, but this might be a reflection of the overall defect in B cell production observed in these animals. In keeping with a possible link to PKC, peripheral B cells in these mice exhibit a defect in anti-IgM-mediated proliferation. These studies suggest that PKK may be required early in B cell development and for BCR-mediated B cell proliferation.

This article has been cited by other articles:

				S. T. Moran, A. Cariappa, H. Liu, B. Muir, D. Sgroi, C. Boboila, and S. Pillai Synergism between NF-{kappa}B1/p50 and Notch2 during the Development of Marginal Zone B Lymphocytes J. Immunol., July 1, 2007; 179(1): 195 - 200. [Abstract] [Full Text] [PDF]

				M. S. Vivarelli, D. McDonald, M. Miller, N. Cusson, M. Kelliher, and R. S. Geha RIP Links TLR4 to Akt and Is Essential for Cell Survival in Response to LPS Stimulation J. Exp. Med., August 2, 2004; 200(3): 399 - 404. [Abstract] [Full Text] [PDF]