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Repression of phospho-JNK and infarct volume in ischemic brain of JIP1-deficient mice

Title
Repression of phospho-JNK and infarct volume in ischemic brain of JIP1-deficient mice
Authors
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
한평림
SCOPUS Author ID
한평림scopus
Issue Date
2003
Journal Title
Journal of Neuroscience Research
ISSN
0360-4012JCR Link
Citation
vol. 74, no. 2, pp. 326 - 332
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
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. [2001] J. Biol. Chem. 276:27745-27748). In contrast, another group (Whitmarsh et al. [2001] 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.
DOI
10.1002/jnr.10761
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일반대학원 > 뇌·인지과학과 > Journal papers
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