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J. Biol. Chem., Vol. 275, Issue 32, 24547-24551, August 11, 2000

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Synergistic Activation of NF-B by Functional Cooperation between Vav and PKC in T Lymphocytes^*

Oliver Dienz, Steffen P. Hehner, Wulf Dröge, and M. Lienhard Schmitz

From the German Cancer Research Center, Department of Immunochemistry (G0200), Im Neuenheimer Feld 280, 69120 Heidelberg, Germany

Here we identified PKC as an activator of transcription factor NF-B in T cells. PKC-induced NF-B activation was synergistically augmented by Vav. Several experimental approaches revealed that PKC is located downstream from Vav in the control of the pathway leading to synergistic NF-B activation. In addition to the synergistic activation cascade, Vav also triggered NF-B activity on a separate route. CD3/CD28-induced activation of NF-B was inhibited by dominant negative forms of Vav or PKC, revealing their essential role in this activation pathway. The Vav/PKC-mediated signals preferentially activated IB kinase . Vav and PKC were found to be constitutively associated in unstimulated T cells. Only the ligation of the costimulatory CD28 receptor, but not of the T cell receptor, resulted in the transient dissociation of the Vav-PKC complex. In contrast, T cell receptor/CD28 costimulation resulted in faster dissociation and slower reassociation kinetics.

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