Prime Time for JNK-Mediated Akt Reactivation in Hypoxia-Reoxygenation

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Prime Time for JNK-Mediated Akt Reactivation in Hypoxia-Reoxygenation by James Shaw, and Lorrie A. Kirshenbaum Circulation Research Volume 98(1):7-9 January 6, 2006 Copyright © American Heart Association, Inc. All rights reserved.

Hypoxia-reoxygenation of cardiomyocytes leads to the activation of MAP kinase terminal effector kinases with opposing effects on cell survival. Hypoxia-reoxygenation of cardiomyocytes leads to the activation of MAP kinase terminal effector kinases with opposing effects on cell survival. The ERKs are typically thought to be antiapoptotic, whereas p38 is primarily proapoptotic. The contribution of JNK toward cell survival or cell death is still debated; however, new evidence has emerged supporting a cytoprotective role. Here, JNK-dependent phosphorylation of the Akt/PKB at site T450 during hypoxia-reoxygenation “primes” Akt/PKB for subsequent phosphorylation at Ser 473 and Thr 308 by the kinases PDK1/2 activating Akt/PKB and cell survival. James Shaw, and Lorrie A. Kirshenbaum Circ Res. 2006;98:7-9 Copyright © American Heart Association, Inc. All rights reserved.