Full metadata record
DC Field | Value | Language |
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dc.contributor.author | 한평림 | - |
dc.date.accessioned | 2016-08-28T11:08:28Z | - |
dc.date.available | 2016-08-28T11:08:28Z | - |
dc.date.issued | 2003 | - |
dc.identifier.issn | 0360-4012 | - |
dc.identifier.other | OAK-1654 | - |
dc.identifier.uri | https://dspace.ewha.ac.kr/handle/2015.oak/219302 | - |
dc.description.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. | - |
dc.language | English | - |
dc.title | Repression of phospho-JNK and infarct volume in ischemic brain of JIP1-deficient mice | - |
dc.type | Article | - |
dc.relation.issue | 2 | - |
dc.relation.volume | 74 | - |
dc.relation.index | SCI | - |
dc.relation.index | SCIE | - |
dc.relation.index | SCOPUS | - |
dc.relation.startpage | 326 | - |
dc.relation.lastpage | 332 | - |
dc.relation.journaltitle | Journal of Neuroscience Research | - |
dc.identifier.doi | 10.1002/jnr.10761 | - |
dc.identifier.wosid | WOS:000185692900017 | - |
dc.identifier.scopusid | 2-s2.0-0141593385 | - |
dc.author.google | Im J.-Y. | - |
dc.author.google | Lee K.-W. | - |
dc.author.google | Kim M.H. | - |
dc.author.google | Lee S.H. | - |
dc.author.google | Ha H.-Y. | - |
dc.author.google | Cho I.-H. | - |
dc.author.google | Kim D. | - |
dc.author.google | Yu M.S. | - |
dc.author.google | Kim J.-B. | - |
dc.author.google | Lee J.-K. | - |
dc.author.google | Kim Y.J. | - |
dc.author.google | Youn B.-W. | - |
dc.author.google | Yang S.-D. | - |
dc.author.google | Shin H.-S. | - |
dc.author.google | Han P.-L. | - |
dc.contributor.scopusid | 한평림(7201947605) | - |
dc.date.modifydate | 20230901081001 | - |