Disease relevance of Mapk10

• In contrast, targeted deletion of Jnk3 not only reduces the stress-induced JNK activity, but also protects mice from brain injury after cerebral ischemia-hypoxia [1].
• We have investigated the effect of JNK1 ko, JNK2 ko, JNK3 ko, JNK2+3 ko and c-JunAA mutation on neuronal survival in adult transgenic mice following ischemia, 6-hydroxydopamine induced neurotoxicity, axon transection and kainic acid induced excitotoxicity [2].

High impact information on Mapk10

• Mice lacking individual members of the Jnk family (Jnk1, Jnk2, and Jnk3) are viable and survive without overt structural abnormalities [3].
• We found that syd and JNK3 are present on vesicular structures in axons, are transported in both the anterograde and retrograde axonal transport pathways, and interact with kinesin-I and the dynactin complex [4].
• Our data revealed that JNK2- and JNK3-induced COX-2 may be a principle pathway responsible for neurodegeneration in PD [5].
• A critical role of neural-specific JNK3 for ischemic apoptosis [1].
• Neural differentiation was observed in wild-type, JNK2(-/-), and JNK3(-/-) cultures but not in JNK1(-/-) EBs [6].

Biological context of Mapk10

• c-Jun N-terminal kinase 3 deficiency protects neurons from axotomy-induced death in vivo through mechanisms independent of c-Jun phosphorylation [7].
• Here, we report that oxidative stress in neurons from JNK3-deficient mice is normal after NGF deprivation [8].

Anatomical context of Mapk10

• Therefore, we have investigated the contractility of blood vessels in mice with genetically deleted JNK1, JNK2, JNK3 and JNK2+3 isoforms and their respective wildtypes [9].
• Following transection of the medial forebrain bundle, however, JNK3 ko conferred persisting neuroprotection of axotomised SNC neurons [2].
• Survival of dopaminergic neurons in the substantia nigra compacta (SNC) following intrastriatal injection of 6-hydroxydopamine was transiently improved in JNK3 ko and c-JunAA mice after 7 days, but not 60 days [2].
• Robust interaction of free arrestins with JNK3 and Mdm2 and their ability to regulate subcellular localization of these proteins may play an important role in the survival of photoreceptors and other neurons, as well as in retinal and neuronal degeneration [10].

Associations of Mapk10 with chemical compounds

• Retinoic acid dramatically increased the expression of JSAP1 and JNK3, which were co-precipitated with anti-JNK3 in the neuroectoderm of wild type but not JSAP1-null embryoid bodies [11].
• JNK3 ko mice were substantially resistant against and survived kainic acid-induced seizures [2].
• JNK3 contributes to c-jun induction and apoptosis in 4-hydroxynonenal-treated sympathetic neurons [12].

Other interactions of Mapk10

• We conclude that endogenous AICD undergoes tight temporal regulation during the differentiation of neurons and is negatively regulated by JNK3 via phosphorylation of APP at Thr668 [13].

Analytical, diagnostic and therapeutic context of Mapk10

• In a sciatic axotomy model of neuronal injury in the neonate, death of DRG neurons was also reduced by JNK3 deficiency [7].
• SAPKbeta/JNK3 is present at levels that are 1/100-1/1,000 those of the positive control and in some cases at the apparent level of the negative control (previously measured by the less-sensitive Northern blot analysis) [14].

References