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A correction to this article has been published: J. Exp. Med. 191 (9) 1389-1390
Published online 19 June 2000.
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© The Rockefeller University Press, 0022-1007/2000/6/2075/ $5.00
The Journal of Experimental Medicine, Volume 191, Number 12, June 19, 2000 2075-2082

Original Article

Protein Kinase D: A Selective Target for Antigen Receptors and a Downstream Target for Protein Kinase C in Lymphocytes



Sharon A. Matthewsa, Enrique Rozengurtb, and Doreen Cantrella

a Lymphocyte Activation Laboratory, Imperial Cancer Research Fund, London WC2A 3PX, United Kingdom
b Department of Medicine, University of California Los Angeles School of Medicine and Molecular Biology Institute, Los Angeles, California 90095-1786
Lymphocyte Activation Laboratory, Rm. 106, Imperial Cancer Research Fund, 44 Lincoln's Inn Fields, London WC2A 3PX, UK.44-020-7269-283144-020-7269-3307

d.cantrell{at}icrf.icnet.uk

Protein kinase Cs (PKCs) are activated by antigen receptors in lymphocytes, but little is known about proximal targets for PKCs in antigen receptor–mediated responses. In this report, we define a role for diacylglycerol-regulated PKC isoforms in controlling the activity of the serine/threonine kinase protein kinase D (PKD; also known as PKCµ) in T cells, B cells, and mast cells. Antigen receptor activation of PKD is a rapid and sustained response that can be seen in T cells activated via the T cell antigen receptor, B cells activated via the B cell antigen receptor, and in mast cells triggered via the high-affinity receptor for IgE (Fc{varepsilon}R1). Herein, we show that antigen receptor activation of PKD requires the activity of classical/novel PKCs. Moreover, PKC activity is sufficient to bypass the requirement for antigen receptor signals in the induction of PKD activity. These biochemical and genetic studies establish a role for antigen receptor–regulated PKC enzymes in the control of PKD activity. Regulation of PKD activity through upstream PKCs reveals a signaling network that exists between different members of the PKC superfamily of kinases that can operate to amplify and disseminate antigen receptor signals generated at the plasma membrane.

Key Words: antigen receptor • diacylglycerol • protein kinase C • protein kinase D

Abbreviations used in this paper: BCR, B cell antigen receptor; Erk, extracellular signal–regulated kinase; GFP, green fluorescent protein; PLC, phospholipase C; PKC, protein kinase C; PKD, protein kinase D; RBL, rat basophilic leukemia.

© 2000 The Rockefeller University Press


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