| First Author | Im JY | Year | 2003 |
| Journal | J Neurosci Res | Volume | 74 |
| Issue | 2 | Pages | 326-32 |
| PubMed ID | 14515362 | Mgi Jnum | J:104842 |
| Mgi Id | MGI:3612907 | Doi | 10.1002/jnr.10761 |
| Citation | Im JY, et al. (2003) Repression of phospho-JNK and infarct volume in ischemic brain of JIP1-deficient mice. J Neurosci Res 74(2):326-32 |
| abstractText | 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. |
