TI - ER-alpha36 mediates testosterone-stimulated Akt activation . AB - The serine/threonine kinase Akt or protein kinase B , plays an important role in cell proliferation and survival [23] . We then tested whether testosterone treatment induces Akt activation in Hec1A cells . As shown in Figure 3A , testosterone treatment induced the rapid PHOSphorylation of Akt . Furthermore , testosterone induced dose -dependent increase in Akt PHOSphorylation (Figure 3B) . ER-alpha36 knockdown was able to abrogate testosterone-induced Akt PHOSphorylation , indicating the involvement of ER-alpha36 (Figure 3C) . Pretreatment of Hec1A cells with the PI3K inhibitor LY294002 effectively inhibited Akt activation stimulated by testosterone (Figure 3D) , indicating that testosterone regulates Akt PHOSphorylation through PI3K . Thus , our data indicated that ER-alpha36 is involved in testosterone-induced Akt activation .