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. 2018 Nov 15;10(11):3413–3429.

Figure 8.

Figure 8

JAK2 overexpression alleviates C2C12 myoblasts I/R injury through the AKT and ERK1/2 pathway. As JAK2 is overexpressed in C2C12 myoblasts cells, the same extracellular stimuli will activate more JAK2, leading to its phosphorylation. Phosphorylated JAK2 can activate PI3K and Ras but without STAT3, resulting in activation of the AKT and ERK1/2 signaling pathway, which further activates mTOR and promotes Bcl-2, Bcl-XL and CREB up-regulation and caspase 9 down-regulation, contributing to inhibition of autophagy and apoptosis and thus making JAK2 perform an important protective role in I/R injury. (Bad: Bcl-xL/Bcl-2-associated death promoter; CREB: cAMP regulatory-binding protein; Bcl-2: B-cell lymphoma-2; Bcl-XL: B-cell lymphoma-extra large).