Premium
Differences in activation of ERK1/2 and p38 kinase in Jnk3 null mice following KA treatment
Author(s) -
De Lemos Luisa,
Junyent Fèlix,
Verdaguer Ester,
Folch Jaume,
Romero Rafael,
Pallàs Mercè,
Ferrer Isisdre,
Auladell Carme,
Camins Antoni
Publication year - 2010
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.2010.06853.x
Subject(s) - neuroprotection , kinase , p38 mitogen activated protein kinases , kainic acid , mapk/erk pathway , ask1 , biology , microbiology and biotechnology , mitogen activated protein kinase , protein kinase a , neuroscience , signal transduction , mitogen activated protein kinase kinase , biochemistry , glutamate receptor , receptor
J. Neurochem. (2010) 114 , 1315–1322. Abstract The MAPK family is formed by extracellular signal‐regulated kinases p38 kinase and stress‐activated protein kinases (SAPK/JNK). There are three genes that encode for three JNK proteins. JNK3 is mainly expressed in the central nervous system and has been related to various processes in that tissue. Specifically, JNK3 plays a crucial role in neuronal death in several neurodegenerative diseases. The activation of this kinase has been described in epilepsy, Alzheimer’s disease, Parkinson’s disease and Huntington’s disease. Different studies have shown that the lack of the Jnk3 gene confers neuroprotection. However, the specific mechanism involved in such neuroprotection has not yet been elucidated. Therefore, in the present study, we analyzed the neuroprotection in mice lacking Jnk3 against neuronal death induced by kainic acid. Moreover, we analyzed the activation of different MAPKs. The results revealed that neuronal death was attenuated and different activation/inactivation of p38 and extracellular signal‐regulated kinases 1/2 was reported with respect to control. Therefore, the data indicate that the lack of the JNK3 protein modulates other MAPKs and these changes could also have a pivotal role in neuroprotection.