| First Author | Martin P | Year | 2002 |
| Journal | EMBO J | Volume | 21 |
| Issue | 15 | Pages | 4049-57 |
| PubMed ID | 12145205 | Mgi Jnum | J:115563 |
| Mgi Id | MGI:3691931 | Doi | 10.1093/emboj/cdf407 |
| Citation | Martin P, et al. (2002) Role of zeta PKC in B-cell signaling and function. EMBO J 21(15):4049-57 |
| abstractText | 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. |
