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. Author manuscript; available in PMC: 2017 Apr 15.
Published in final edited form as: Mol Cell Endocrinol. 2015 Dec 28;425:48–60. doi: 10.1016/j.mce.2015.12.006

Figure 2. Effect of pharmacological pan-PKC inhibitor Bisindolylmaleimide (BIS) on IGFBP-1 phosphorylation.

Figure 2

HepG2 cells were treated with BIS (7.5 μM) and cultured in leucine plus (450 μM) or in leucine deprived (0 μM) media for 24 hours (n=3 each). A representative western immunoblot of HepG2 cell media indicating A. total IGFBP-1 and B. IGFBP-1 phosphorylation at Ser101, Ser119 and Ser169 in leucine plus (450 μM), leucine deprivation, BIS, and leucine deprivation+BIS treatments. Inhibition of PKC in leucine deprivation attenuates IGFBP-1 hyperphosphorylation at Ser101, Ser119 and Ser169. Values are displayed as mean + SEM. *p< 0.05, **p= 0.001-0.05, ***p < 0.0001 versus control; One-way analysis of variance; Dunnet’s Multiple Comparison Test; n=3. C:450 Control, 450 μM leucine. C:0: Leucine deprivation, 0 μM leucine. BIS:450: Bisindolylmaleimide (7.5 μM), 450 μM leucine. BIS:0: Bisindolylmaleimide (7.5 μM), 0 μM leucine.