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Dopamine induces a PI3-kinase-independent activation of Akt in striatal neurons: a new route to cAMP response element-binding protein phosphorylation

By Karen Brami-cherrier, Emmanuel Valjent, Marta Garcia, Christiane Pagès, Robert A. Hipskind and Jocelyne Caboche

Abstract

Akt is classically described as a prosurvival serine/threonine kinase activated in response to trophic factors. After activation by phosphoinositide 3-kinase (PI3-kinase), it can translocate to the nucleus where it promotes specific genetic programs by catalyzing phosphorylation of transcription factors. We report here that both dopamine (DA) D1 (SKF38393) and D2 (quinpirole) agonist treatments rapidly increase, in primary striatal neurons in culture, phosphorylation levels of Akt on Thr 308,a residue that is critically involved in its kinase activity. These treatments also activate the extracellular signal-regulated kinase (ERK) pathway in the same population of striatal neurons. Induction of active, phospho-Thr 308 Akt by dopamine D1 and D2 agonists is insensitive to wortmannin and thus PI3-kinase independent, in contrast to growth factor-induced Akt activity. D1- and D2-induced phospho-Thr 308 Akt is decreased by th

Topics: Key words, extracellular signal-regulated
Year: 2002
OAI identifier: oai:CiteSeerX.psu:10.1.1.319.1191
Provided by: CiteSeerX
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