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. 2017 Jan 23;13(1):e1006147. doi: 10.1371/journal.ppat.1006147

Fig 5. Complex formation induces ERK2, JNK and AKT pathways in Xenopus oocytes in a ligand-independent way.

Fig 5

Western blot analyses of signaling pathways triggered by Smβ-Int1 complex-mediated SmVKR1 activation in Xenopus oocytes. The schistosome complex members were expressed in Xenopus oocytes for 5 h with or without ligand. Oocyte lysates were analyzed to investigate the phosphorylation state of ERK2, JNK and AKT following SmVKR1- Smβ-Int1 complex formation. In the absence of L-Arg as ligand, and in case of the combination of Smβ-Int1, SmILK, SmPINCH, SmNck2, and SmVKR1 (lane 1) phosphorylation of ERK2 (ERK2P), JNK (JNKP), and AKT (AKTP) was observed. In cases of using mutated forms (SmILKΔAnk1, lane 2; SmPINCHΔLIM1, lane 3; SmPINCHΔLIM4, lane 4; SmNck2ΔSH3, laneΔ 5; SmVKR1 KO, lane 6) or the ILK inhibitor QLT-0267 (1 μM; lane 7), no phosphorylation of ERK2, JNK, and AKT was detected. As expected, phosphorylation of ERK2, JNK, and AKT was observed in SmVKR1-expressing oocytes stimulated by L-Arg (1 μM), which served as positive control (lane 8).