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Akt suppresses androgen-induced apoptosis by phosphorylating and inhibiting androgen receptor.

http://www.ncbi.nlm.nih.gov/pubmed/11404460

Whereas several apoptosis-related proteins have been linked to the antiapoptotic effects of Akt serine-threonine kinase, the search continues to explain the Akt signaling role in promoting cell survival via antiapoptotic effects. Here, we demonstrate that Akt phosphorylates the androgen receptor (AR) at Ser-210 and Ser-790. A mutation at AR Ser-210 results in the reversal of Akt-mediated suppression of AR transactivation. Activation of the phosphatidylinositol-3-OH kinase/Akt pathway results in the suppression of AR target genes, such as p21, and the decrease of androgen/AR-mediated apoptosis, which may involve the inhibition of interaction between AR and AR coregulators. Together, these findings provide a molecular basis for cross-talk between two signaling pathways at the level of Akt and AR-AR coregulators that may help us to better understand the roles of Akt in the androgen/AR-mediated apoptosis.

Pubmed ID: 11404460 RIS Download

Mesh terms: Amino Acid Substitution | Androgen Receptor Antagonists | Apoptosis | Chromones | Dihydrotestosterone | Enzyme Inhibitors | Gene Expression Regulation, Neoplastic | Humans | Male | Morpholines | Mutagenesis, Site-Directed | Phosphatidylinositol 3-Kinases | Phosphorylation | Prostatic Neoplasms | Protein-Serine-Threonine Kinases | Proto-Oncogene Proteins | Proto-Oncogene Proteins c-akt | Receptors, Androgen | Recombinant Proteins | Serine | Signal Transduction | Transcriptional Activation | Transfection | Tumor Cells, Cultured

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