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. 2016 Jul 28;99(2):443–450. doi: 10.1016/j.ajhg.2016.06.010

Figure 4.

Figure 4

GNA14 and GNA11 Mutations Upregulate the MAPK Pathway in NBMELs and HUVECs Independently of AKT Activation

Activating mutations in GNA14 and GNA11 upregulate phosphorylation of ERK1/2 in NBMELs (left) and HUVECs (right). GNA14 p.Arg179Cys and GNA11 p.Arg183Cys induce lower p-ERK levels in both cell types than do GNA14 p.Gln205Leu and GNA11 p.Gln209Pro. The membranes were probed with antibodies against GNA11 (D-17, Santa Cruz), GNA14 (SAB4300771, Sigma-Aldrich), BRAF (AF3424, R&D), KRAS (3B10-2F2 WH0003845M1, Sigma-Aldrich), pERK p44/42K T202/Y204 (E10, 9106, Cell Signaling Technology), ERK (4695, Cell Signaling Technology), phospho AKT S473 (9271, Cell Signaling Technology), AKT (9272, Cell Signaling Technology), and β-actin (A1978, Sigma-Aldrich) or tubulin (T5168 Sigma-Aldrich) as controls for protein loading.