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

@article{citeulike:599321, 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.}, address = {Institute of Medical Biology and Human Genetics, University of Innsbruck, Schoepfstrasse 41, A-6020 Innsbruck, Austria.}, author = {Pfeifhofer, C. and Kofler, K. and Gruber, T. and Tabrizi, N. G. and Lutz, C. and Maly, K. and Leitges, M. and Baier, G.}, citeulike-article-id = {599321}, citeulike-linkout-0 = {http://dx.doi.org/10.1084/jem.20020234}, citeulike-linkout-1 = {http://view.ncbi.nlm.nih.gov/pubmed/12782715}, citeulike-linkout-2 = {http://www.hubmed.org/display.cgi?uids=12782715}, day = {2}, doi = {10.1084/jem.20020234}, issn = {0022-1007}, journal = {J Exp Med}, keywords = {calcium, cell, nfat, pkc, t}, month = {June}, number = {11}, pages = {1525--1535}, posted-at = {2006-04-25 08:57:33}, priority = {2}, title = {Protein kinase C theta affects Ca2+ mobilization and NFAT cell activation in primary mouse T cells.}, url = {http://dx.doi.org/10.1084/jem.20020234}, volume = {197}, year = {2003} }

TY - JOUR ID - citeulike:599321 L3 - citeulike-article-id:599321 N2 - 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. IS - 11 JF - J Exp Med SN - 0022-1007 AD - Institute of Medical Biology and Human Genetics, University of Innsbruck, Schoepfstrasse 41, A-6020 Innsbruck, Austria. EP - 1535 TI - Protein kinase C theta affects Ca2+ mobilization and NFAT cell activation in primary mouse T cells. VL - 197 SP - 1525 KW - calcium KW - cell KW - nfat KW - pkc KW - t AU - Pfeifhofer, C AU - Kofler, K AU - Gruber, T AU - Tabrizi, NG AU - Lutz, C AU - Maly, K AU - Leitges, M AU - Baier, G PY - 2003/06/02/ UR - http://dx.doi.org/10.1084/jem.20020234 ER -