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. 2011 Feb 3;25(4):669–680. doi: 10.1210/me.2010-0437

Fig. 2.

Fig. 2.

GnRH uses the same signaling pathways for induction of the c-Fos and FSHβ genes. LβT2 cells were transfected with 1 kb mouse c-Fos-luciferase (A and D); 1 kb mouse FSHβ-luciferase (B and E), or 1 kb mouse Egr-1-luciferase (C), and then treated with 10 nm GnRH for 5 h. BAPTA (B, 50 μm) (to chelate intracellular calcium), 1 μm BIM (to inhibit PKC), 10 μm H89 (to inhibit PKA), 10 μm KN-93 (KN; to inhibit CamKII), 50 μm LY 294002 (LY; to inhibit phosphatidylinositol 3 kinase), 5 μm UO126 (UO; to inhibit MEK1 and activation of ERK1/2), 20 μm SB 202190 (SB; to inhibit p38), or 10 μm SP 600125 (JNK; to inhibit JNK), were added to cells as indicated 10 min before hormone treatment. The results were represented as fold induction by GnRH relative to the control cells treated with the same inhibitor; *, Significant decrease in fold induction from GnRH-treated cells without inhibitor (ctrl); P < 0.05. ctrl, Control.