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. 2013 Jan 2;14:1. doi: 10.1186/1471-2202-14-1

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Copyright ©2013 Zhu et al; licensee BioMed Central Ltd.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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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.