Alleviating the Suppression of Glycogen Synthase Kinase-3β by Akt Leads to the Phosphorylation of cAMP-response Element-binding Protein and Its Transactivation in Intact Cell Nuclei
Open Access
- 1 October 2003
- journal article
- Published by Elsevier
- Vol. 278 (42) , 41338-41346
- https://doi.org/10.1074/jbc.m302972200
Abstract
No abstract availableKeywords
This publication has 44 references indexed in Scilit:
- Multiple Phosphoinositide 3-Kinase-Dependent Steps in Activation of Protein Kinase BMolecular and Cellular Biology, 2002
- The Phosphoinositide 3-Kinase PathwayScience, 2002
- Resistance of prostate cancer cells to soluble TNF-related apoptosis-inducing ligand (TRAIL/Apo2L) can be overcome by doxorubicin or adenoviral delivery of full-length TRAILCancer Gene Therapy, 2002
- The renaissance of GSK3Nature Reviews Molecular Cell Biology, 2001
- PKB/AKT: functional insights from genetic modelsNature Reviews Molecular Cell Biology, 2001
- Constitutively active Akt is an important regulator of TRAIL sensitivity in prostate cancerOncogene, 2001
- The multifaceted roles of glycogen synthase kinase 3β in cellular signalingPublished by Elsevier ,2001
- Differential Effects of Phosphatidylinositol-3/Akt-Kinase Inhibition on Apoptotic Sensitization to Cytokines in LNCaP and PC-3 Prostate Cancer CellsJournal of Interferon & Cytokine Research, 2001
- Tyrosine dephosphorylation of glycogen synthase kinase‐3 is involved in its extracellular signal‐dependent inactivationFEBS Letters, 1996
- Inhibition of glycogen synthase kinase-3 by insulin mediated by protein kinase BNature, 1995