Interleukin-3-Induced Phosphorylation of BAD Through the Protein Kinase Akt
Copyright policy )Interleukin-3-Induced Phosphorylation of BAD Through the Protein Kinase Akt
BAD is a distant member of the Bcl-2 family that promotes cell death. Phosphorylation of BAD prevents this. BAD phosphorylation induced by interleukin-3 (IL-3) was inhibited by specific inhibitors of phosphoinositide 3-kinase (PI 3-kinase). Akt, a survival-promoting serine-threonine protein kinase, was activated by IL-3 in a PI 3-kinase–dependent manner. Active, but not inactive, forms of Akt were found to phosphorylate BAD in vivo and in vitro at the same residues that are phosphorylated in response to IL-3. Thus, the proapoptotic function of BAD is regulated by the PI 3-kinase–Akt pathway.
- University of Michigan–Ann Arbor United States
- Parke-Davis United States
- University of Michigan–Flint United States
Morpholines, Apoptosis, Protein Serine-Threonine Kinases, Cell Line, Androstadienes, Enzyme Activation, Mice, Phosphatidylinositol 3-Kinases, Phosphoserine, Proto-Oncogene Proteins c-bcl-2, Chromones, Proto-Oncogene Proteins, Animals, Humans, Interleukin-3, Enzyme Inhibitors, Phosphorylation, Carrier Proteins, Proto-Oncogene Proteins c-akt, Phosphoinositide-3 Kinase Inhibitors
Morpholines, Apoptosis, Protein Serine-Threonine Kinases, Cell Line, Androstadienes, Enzyme Activation, Mice, Phosphatidylinositol 3-Kinases, Phosphoserine, Proto-Oncogene Proteins c-bcl-2, Chromones, Proto-Oncogene Proteins, Animals, Humans, Interleukin-3, Enzyme Inhibitors, Phosphorylation, Carrier Proteins, Proto-Oncogene Proteins c-akt, Phosphoinositide-3 Kinase Inhibitors
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