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. 2012 Sep 26;26(12):2046–2057. doi: 10.1210/me.2012-1171

Fig. 4.

Fig. 4.

Calcium and the MEK/ERK1/2 pathway regulate TSHR expression in FRTL-5 cells. A, Treating FRTL-5 cells with EGTA (5 mm, 24 h) elevated pERK (n = 4, P < 0.001) and also increased TSHR expression (n = 4, P < 0.001). B, Transient expression of truncated (dominant-negative) TRPC2 construct (TRPC2DN) increased both pERK and TSHR (n = 4, P < 0.05 and n = 6, P < 0.01, respectively). C, The TRPC2DN construct reduced ATP-induced calcium transients as compared with YFP-transfected controls. D, Quantification of results from C, bars indicate means ± sem, n ≥ 35; **, P < 0.01. E, Inhibiting MEK with U0126 (10 μm, 24 h) reduced both pERK1/2 (n = 3, P < 0.05) and the TSHR (n = 4, P < 0.01) in native FRTL-5 cells. F, Transient expression of a constitutively active MEK1 mutant (MEK1–S218E/S222D) in FRTL-5 cells increased pERK (n = 3, P < 0.05), whereas transient expression of a catalytically inactive mutant (MEK1–K97M) had no significant effect. Relative band densities are included above the representative Western blottings.