Figure 7.

Model of JNK inhibition after cerebral ischemia/reperfusion. JNK activity can be elevated by activated ASK-SEK1 or MLK3-MKK-7, or be downregulated by dephosphorylation of JNK at Thr183/Tyr185 by specific phosphatases MKP-7 following ischemia/reperfusion. MKP-7 function is increased by its nuclear-to-cytoplasmic translocation, which ultimately inhibits JNK activity. Active Akt (which inactivates SEK1 by phosphorylation Ser80 and inhibits MKK-7 by MLK3 phosphorylation at Ser674) does not affect down-regulation of JNK activity induced by MKP-7 after ischemia in the rat hippocampus.

Zhu et al. BMC Neuroscience 2013 14:1   doi:10.1186/1471-2202-14-1
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