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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 [OPEN ACCESS]
Web of Science PubMed PUBMED Central FullText FullText_MUG

 

Co-authors Med Uni Graz
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)
Animals -
Base Sequence -
Calcium Signaling -
Cells, Cultured -
DNA - genetics
DNA-Binding Proteins - genetics
Isoenzymes - deficiency
Lymphocyte Activation - deficiency
Mice - deficiency
Mice, Knockout - deficiency
NF-kappa B - metabolism
NFATC Transcription Factors - metabolism
Nuclear Proteins - metabolism
Protein Kinase C - deficiency
Receptor-CD3 Complex, Antigen, T-Cell - metabolism
T-Lymphocytes - cytology
Transcription Factors - genetics
Transcriptional Activation - genetics

Find related publications in this database (Keywords)
T lymphocyte
PKC theta
TCR/CD3
Ca2+ response
NFAT
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