The Akt activation inhibitor TCN-P inhibits Akt phosphorylation by binding to the PH domain of Akt and blocking its recruitment to the plasma membrane

Persistently hyper-phosphorylated Akt contributes to human oncogenesis and resistance to therapy. TCN-P, the active metabolite of the Akt phosphorylation inhibitor triciribine (TCN), is in clinical trials, but the mechanism by which TCN-P inhibits Akt phosphorylation is unknown. Here we show that in...

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Hlavní autoři: Berndt, Norbert, Yang, Hua, Trinczek, Bernhard, Betzi, Stéphane, Zhang, Ziming, Wu, Bainan, Lawrence, Nicholas J., Pellecchia, Maurizio, Schönbrunn, Ernst, Cheng, Jin Q., Sebti, Saïd M.
Médium: Artigo
Jazyk:Inglês
Vydáno: 2010
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Article
On-line přístup:https://ncbi.nlm.nih.gov/pmc/articles/PMC2952662/
https://ncbi.nlm.nih.gov/pubmed/20489726
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1038/cdd.2010.63
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