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J Exp Med. 2003 Jun 2;197(11):1525-35.

Protein kinase C theta affects Ca2+ mobilization and NFAT cell activation in primary mouse T cells.

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Institute of Medical Biology and Human Genetics, University of Innsbruck, Schoepfstrasse 41, A-6020 Innsbruck, Austria.

Erratum in

  • J Exp Med. 2003 Jul 7;198(1):183.


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.

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