Figure 5

Suggested pathways through which Src kinase regulates cell proliferation in the DG after ischemia. Transient global ischemia triggered sustained activation of Src kinase by intracellular Ca²⁺ influx via NMDA and L-VGCC or released from ER and mitochondria. Subsequently, activated Src induced continuous phosphorylation of ERK through direct phosphorylation of Raf-1 at its Tyr 340/341, and in turn, was translocated from the cytosol to the nucleus where it regulated transcription via CREB and some genes relating to cell proliferation expression.