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. 2023 Apr 12;299(5):104699. doi: 10.1016/j.jbc.2023.104699

Figure 8.

Figure 8

Model of the non-canonical activation of EphA2 by typically or atypically activated RSK. Upon the stimulation of growth factors, ERK typically activates CTK to induce the activation of NTK, resulting in the non-canonical activation of EphA2. On the other hand, cellular stress-activated MK2 catalyzes the phosphorylation of RSK1 at Ser-380 to induce NTK activation in a CTK-independent manner. This atypically activated RSK also induces the non-canonical activation of EphA2 to promote cancer malignancy. CTK, carboxyl-terminal kinase; EphA2, ephrin type-A receptor 2; ERK, extracellular signal-regulated kinase; MK2, MAPK-activated protein kinase 2; NTK, amino-terminal kinase; RSK, p90 ribosomal S6 kinase.