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Repression of phospho-JNK and infarct volume in ischemic brain of JIP1-deficient mice
- Repression of phospho-JNK and infarct volume in ischemic brain of JIP1-deficient mice
- Im J.-Y.; Lee K.-W.; Kim M.H.; Lee S.H.; Ha H.-Y.; Cho I.-H.; Kim D.; Yu M.S.; Kim J.-B.; Lee J.-K.; Kim Y.J.; Youn B.-W.; Yang S.-D.; Shin H.-S.; Han P.-L.
- Ewha Authors
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- Journal of Neuroscience Research
- Journal of Neuroscience Research vol. 74, no. 2, pp. 326 - 332
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- Mice lacking JIP1, a scaffold protein that organizes JNK pathway components, were constructed independently by two groups. The proposed in vivo function, however, remains contradictory; One study reported that targeted disruption of the jip1 caused embryonic death due to the requirement of JIP1 for fertilized eggs (Thompson et al.  J. Biol. Chem. 276:27745-27748). In contrast, another group (Whitmarsh et al.  Genes Dev. 15: 2421-2432) demonstrated that JIP1-deficient mice were viable and that the JIP1 null mutation inhibited the kainic acid-induced JNK activation and neuronal death. The current study was undertaken to re-elucidate the in vivo roles of JIP1 using newly generated JIP1 knockout mice. Our JIP1-deficient mice were viable and healthy. The transient focal ischemic insult produced by middle cerebral artery occlusion (MCAO) strongly activated JNK in brain of jip1 +/+, jip1 +/, and jip1 -/- mice. Increased JNK activity was sustained for more than 22 hr in jip1 +/+ and jip1 +/-, whereas it was repressed rapidly in jip1 -/-. Concomitantly, the infarct volume produced by the ischemic insult in jip1 -/- was reduced notably compared to that in jip1 +/+ brain. These results suggest that JIP1 plays a pivotal role in regulating the maintenance of phosphorylated JNK and neuronal survival in postischemic brain, but is not essential for JNK activation and early development. © 2003 Wiley-Liss, Inc.
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