| First Author | Pfeifhofer C | Year | 2003 |
| Journal | J Exp Med | Volume | 197 |
| Issue | 11 | Pages | 1525-35 |
| PubMed ID | 12782715 | Mgi Jnum | J:83733 |
| Mgi Id | MGI:2663371 | Doi | 10.1084/jem.20020234 |
| Citation | Pfeifhofer C, et al. (2003) Protein kinase C theta affects Ca2+ mobilization and NFAT cell activation in primary mouse T cells. J Exp Med 197(11):1525-35 |
| abstractText | Protein kinase C (PKC)theta is an established component of the immunological synapse and has been implicated in the control of AP-1 and NF-kappaB. To study the physiological function of PKCtheta, we used gene targeting to generate a PKCtheta null allele in mice. Consistently, interleukin 2 production and T cell proliferative responses were strongly reduced in PKCtheta-deficient T cells. Surprisingly, however, we demonstrate that after CD3/CD28 engagement, deficiency of PKCtheta primarily abrogates NFAT transactivation. In contrast, NF-kappaB activation was only partially reduced. This NFAT transactivation defect appears to be secondary to reduced inositol 1,4,5-trisphosphate generation and intracellular Ca2+ mobilization. Our finding suggests that PKCtheta plays a critical and nonredundant role in T cell receptor-induced NFAT activation. |
