Selected Publication:
Pfeifhofer, C; Kofler, K; Gruber, T; Tabrizi, NG; Lutz, C; Maly, K; Leitges, M; Baier, G.
Protein kinase C theta affects Ca2+ mobilization and NFAT cell activation in primary mouse T cells.
J Exp Med. 2003; 197(11):1525-1535
Doi: 10.1084/jem.20020234
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- Co-authors Med Uni Graz
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Ghaffari Tabrizi-Wizsy Nassim
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- Abstract:
- 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.
- Find related publications in this database (using NLM MeSH Indexing)
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Animals -
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Base Sequence -
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Calcium Signaling -
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Cells, Cultured -
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DNA - genetics
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DNA-Binding Proteins - genetics
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Isoenzymes - deficiency
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Lymphocyte Activation - deficiency
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Mice - deficiency
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Mice, Knockout - deficiency
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NF-kappa B - metabolism
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NFATC Transcription Factors - metabolism
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Nuclear Proteins - metabolism
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Protein Kinase C - deficiency
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Receptor-CD3 Complex, Antigen, T-Cell - metabolism
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T-Lymphocytes - cytology
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Transcription Factors - genetics
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Transcriptional Activation - genetics
- Find related publications in this database (Keywords)
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T lymphocyte
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PKC theta
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TCR/CD3
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Ca2+ response
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NFAT