Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P05412 (c-Jun)
 11,453 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this study we investigated the effects of deltamethrin on the expression of c-Fos and c-Jun in the cerebral cortex of rats. Immunohistochemical analysis demonstrated that the immunoreactivity for c-Fos was markedly increased in the cerebral cortex 5 h after deltamethrin treatment, and maintained at an increased level at 24 h, even though little immunoreactivity for c-Fos was seen in the same brain region of control rats. The immunostaining for c-Jun was also dramatically elevated in the same brain region, showing the same time course of c-Fos expression after deltamethrin treatment. Further, both MK-801, an N-methyl-D-aspartate (NMDA) receptor antagonist, and NBQX, an alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA)/kainate (KA) receptor antagonist, attenuated deltamethrin-elicited prolonged expression of c-Fos and c-Jun. Since the persistent expression of c-Fos and c-Jun is unusual, and has been reported before in conditions involving neurodegeneration, our results are consistent with a model that deltamethrin induces neurodegeneration through a glutamate-dependent pathway.
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PMID:Prolonged expression of c-Fos and c-Jun in the cerebral cortex of rats after deltamethrin treatment. 1257 43

In mouse cerebellar granule neurons (CGNs) the marine neurotoxin domoic acid (DomA) induces neuronal cell death, either by apoptosis or by necrosis, depending on its concentration, with apoptotic damage predominating in response to low concentrations (100 nM). DomA-induced apoptosis is due to selective activation of AMPA/kainate receptors, and is mediated by DomA-induced oxidative stress, leading to mitochondrial dysfunction and activation of caspase-3. The p38 MAP kinase and the c-Jun NH2-terminal protein kinase (JNK) have been shown to be preferentially activated by oxidative stress. Here we report that DomA increases p38 MAP kinase and JNK phosphorylation, and that this effect is more pronounced in CGNs from Gclm (-/-) mice, which lack the modifier subunit of glutamate-cysteine ligase, have very low glutathione (GSH) levels, and are more sensitive to DomA-induced apoptosis than CGNs from wild-type mice. The increased phosphorylation of JNK and p38 kinase was paralleled by a decreased phosphorylation of Erk 1/2. The AMPA/kainate receptor antagonist NBQX, but not the NMDA receptor antagonist MK-801, prevents DomA-induced activation of p38 and JNK kinases. Several antioxidants (GSH ethyl ester, catalase and phenylbutylnitrone) also prevent DomA-induced phosphorylation of JNK and p38 MAP kinases. Inhibitors of p38 (SB203580) and of JNK (SP600125) antagonize DomA-induced apoptosis. These results indicate the importance of oxidative stress-activated JNK and p38 MAP kinase pathways in DomA-induced apoptosis in CGNs.
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PMID:Apoptosis induced by domoic acid in mouse cerebellar granule neurons involves activation of p38 and JNK MAP kinases. 1816 2