Role of zeta PKC in B-cell signaling and function.

TitleRole of zeta PKC in B-cell signaling and function.
Publication TypeJournal Article
Year of Publication2002
AuthorsMartin P, Duran A, Minguet S, Gaspar M-L, Diaz-Meco M-T, Rennert P, Leitges M, Moscat J
JournalEMBO J
Volume21
Issue15
Pagination4049-57
Date Published2002 Aug 01
ISSN0261-4189
KeywordsAnimals, Antibody Formation, Apoptosis, B-Lymphocytes, bcl-X Protein, Cell Division, Enzyme Activation, Gene Expression Regulation, I-kappa B Proteins, Immunity, Cellular, Immunologic Deficiency Syndromes, Interleukin-6, Isoenzymes, Lymphoid Tissue, MAP Kinase Signaling System, Mice, Mice, Knockout, Mitogen-Activated Protein Kinase 1, Mitogen-Activated Protein Kinase 3, Mitogen-Activated Protein Kinases, NF-kappa B, Protein Kinase C, Proto-Oncogene Proteins c-bcl-2, Receptors, Antigen, B-Cell, T-Lymphocytes, Transcription, Genetic
Abstract

The atypical protein kinase C isoform, zeta PKC, has been implicated in the control of extracellular signal-regulated kinase (ERK) and nuclear factor (NF)-kappa B pathways. Recent evidence from zeta PKC knock-out mice demonstrates that this kinase is important for NF-kappa B transcriptional activity but not for ERK activation in embryonic fibroblasts. The lack of zeta PKC produces in mice a number of alterations in the development of secondary lymphoid tissues that could be accounted for, at least in part, by defects in B-cell function. Here, we present evidence that the loss of zeta PKC selectively impairs signaling through the B-cell receptor, resulting in inhibition of cell proliferation and survival, as well as defects in the activation of ERK and the transcription of NF-kappa B-dependent genes. Furthermore, zeta PKC-/- mice are unable to mount an optimal T-cell-dependent immune response. Collectively, these results genetically establish a critical role for zeta PKC in B-cell function in vitro and in vivo.

DOI10.1093/emboj/cdf407
Alternate JournalEMBO J
PubMed ID12145205
PubMed Central IDPMC126153
Related Faculty: 
Jorge Moscat, Ph.D. Maria Diaz-Meco Conde, Ph.D.

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