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. 2019 Apr 17;17:37. doi: 10.1186/s12964-019-0351-5

Fig. 6.

Fig. 6

PI3K is a caveolin-1-regulated mediator of PKCζ required for FST upregulation in cav-1 KO MC. a The PI3K inhibitors wortmannin (500 nM) or LY294002 (20 μM), but not the Akt inhibitor Akt VIII (20μM) for 24 h abolished the increased Sp1 activity observed in cav-1 KO vs WT MC (n = 6, *vs WT, # vs KO control, p < 0.05). b PI3K inhibition prevented the increase in FST mRNA expression observed in cav-1 KO MC (n = 5, *vs WT, #vs KO control, p < 0.05). c PI3K inhibition also abolished the increased FST protein expression observed in cav-1 KO vs WT MC (n = 4, *vs WT, #vs KO control, p < 0.05). d Cav-1 WT and KO MC were transfected with the fluorescent PIP3 biosensor PH AKT-Venus (green). Elevated basal PI3K activity, as observed by increased PIP3 production at the plasma membrane, delineated by WGA (red), was seen in cav-1 KO MC. This is highlighted by the white co-localization mask (n = 3, 21 micrographs quantified, with representative micrographs shown)