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J Biol Chem, Vol. 273, Issue 43, 28025-28031, October 23, 1998
,
From the Phosphoinositide (PI) 3-kinase has been
implicated in T cell receptor (TCR) signaling, either as a positive or
a negative regulatory molecule. Here, we show that for normal mouse
lymph node T cells, PI 3-kinase activity is required for interleukin-2 (IL-2) production following TCR-mediated activation. Furthermore, in
normal T cells, inhibition of PI 3-kinase prevented activation of
enzymes in the extracellular signal-regulated protein kinase (ERK)
signaling pathway (MEK-1 and ERK-2). Overexpression of a dominant-negative mutant of PI 3-kinase and pharmacological inhibitors of PI 3-kinase prevented transcriptional activation of AP-1 and NF-AT,
transcription factors regulated by ERK-2 and pivotal for IL-2 gene
expression. Although a constitutively active form of Akt kinase, a
downstream mediator of PI 3-kinase function, enhanced TCR-induced IL-2
gene transcription, it could not bypass the requirement for PI 3-kinase
activity. Therefore, PI 3-kinase is likely to be involved in signaling
for IL-2 production in at least two steps in the TCR-initiated
signaling pathway.
Laboratory of Immune Cell Biology, NCI,
National Institutes of Health, Bethesda, Maryland 20892-1152, the
§ Department of Biochemistry and Molecular Biology,
University of Santiago de Compostela, Santiago de Compostela 15706, Spain, and the ¶ Department of Pharmacology, Columbia University,
New York, New York 10032
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