(PDF) Protein Kinase C-Α Overexpression Stimulates Akt

Protein Kinase C-Α Overexpression Stimulates Akt Activity and Suppresses Apoptosis Induced by Interleukin 3 Withdrawal

Oncogene - United Kingdom

doi 10.1038/sj.onc.1203065

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November 1, 1999

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Springer Science and Business Media LLC

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Protein Kinase C-Α Overexpression Stimulates Akt Activity and Suppresses Apoptosis Induced by Interleukin 3 Withdrawal

Oncogene - United Kingdom

doi 10.1038/sj.onc.1203065

Full Text

Abstract

Categories

Date

Authors

Publisher

Related search

GqProtein-induced Apoptosis Is Mediated by AKT Kinase Inhibition That Leads to Protein Kinase C-Induced C-Jun N-Terminal Kinase Activation

Role of Akt and C-Jun N-Terminal Kinase 2 in Apoptosis Induced by Interleukin-4 Deprivation

Receptor Interacting Protein 3 Suppresses Vascular Smooth Muscle Cell Growth by Inhibition of the Phosphoinositide 3-Kinase-Akt Axis

Overexpression of Protein-Tyrosine Phosphatase-1b in Adipocytes Inhibits Insulin-Stimulated Phosphoinositide 3-Kinase Activity Without Altering Glucose Transport or Akt/Protein Kinase B Activation

Inhibition of Phosphatidylinositol 3-Kinase by PX-866 Suppresses Temozolomide-Induced Autophagy and Promotes Apoptosis in Glioblastoma Cells

Inhibition of Protein Kinase C by Isojacareubin Suppresses Hepatocellular Carcinoma Metastasis and Induces Apoptosis in Vitro and in Vivo

Protein Kinase C Activity and Hexamethylenebisacetamide-Induced Erythroleukemia Cell Differentiation.

Correlation Between Sustained C-Jun N-Terminal Protein Kinase Activation and Apoptosis Induced by Tumor Necrosis Factor-Α in Rat Mesangial Cells

Nuclear Protein Kinase C Isoforms and Apoptosis