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Papers In Press, published online ahead of print June 24, 2003
Laboratory of Neurochemistry, NINDS/NIH, Bethesda, MD 20892
Corresponding Author: panth{at}ninds.nih.gov
The PI-3 kinase/Akt signaling pathway plays an important role in mediating survival signals in wide variety of neurons and cells. Recent studies show that Akt also regulates metabolic pathways to regulate cell survival. In this study, we reported that cyclindependent kinase-5 (Cdk5) regulates Akt activity and cell survival through the neuregulin –mediated PI3-Kinase signaling pathway. We found that brain extracts of Cdk5-/- mice display a lower PI-3 kinase activity and phosphorylation of Akt compared to that in wild type mice. Moreover, we demonstrated that Cdk5 phosphorylated Ser-1176 in the neuregulin receptor ErbB2, and Thr-871 and Ser-1120 in the ErbB3 receptor. We identified the Ser-1120 sequence RSRSPR in ErbB3 as a novel phosphorylation consensus sequence of Cdk5. Finally, we found that Cdk5 activity is involved in neuregulin-induced Akt activity and neuregulin-mediated neuronal survival. These findings suggest that Cdk5 may exert a key role in promoting neuronal survival by regulating Akt activity through the neuregulin/PI3-K signaling pathway.
J. Biol. Chem, 10.1074/jbc.M302004200
Submitted on February 25, 2003
Revised on May 29, 2003
Accepted on June 24, 2003
Cdk5 is involved in neuregulin-dependent activation of PI-3 kinase and Akt activity mediating neuronal survival
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