INT110180
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
AEA triggered phosphorylation of c-Jun NH(2)-terminal kinase (JNK) and p38 mitogen activated protein kinase. | |||||||||||||||
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Extracellular signal-regulated kinase 1 and 2, p38 and stress-activated protein kinase/c-Jun-NH(2)-kinase were not phosphorylated after omega-6 fatty acid addition. | |||||||||||||||
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In the present study we used immunoblotting techniques to examine the effects of acute and repeated restraint stress on the phosphorylation state of three MAPKs, the extracellular signal-regulated kinase Erk1/2, c-Jun-N-terminal kinase/stress-activated protein kinase (JNK/SAPK) and p38 MAPK, in different brain regions. | |||||||||||||||
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p-c-Jun, phosphorylated c-Jun | |||||||||||||||
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The shift of redox balance towards oxidative conditions facilitates phosphorylation and activation of c-Jun N-terminal kinase (JNK), a kinase that promotes Jun translocation into the nucleus. | |||||||||||||||
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p-c-Jun, phosphorylated c-Jun | |||||||||||||||
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Vpr activates the DNA binding activity of AP-1 by promoting the phosphorylation of cFos and cJun in monocytes and macrophages [267]. | |||||||||||||||
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-induced MAPK activation, we investigated the phosphorylation of c-jun amino-terminal kinase (JNK), p38 and extracellular signal-regulated kinase (ERK)1/2 after pretreatment with glucosamine and stimulation with IL-1?. | |||||||||||||||
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Glucosamine inhibited c-jun amino-terminal kinase and p38 phosphorylation, and consequently c-jun binding activity. | |||||||||||||||
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Glucosamine inhibited c-jun amino-terminal kinase and p38 phosphorylation, and consequently c-jun binding activity. | |||||||||||||||
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stimulated phosphorylation of c-jun amino-terminal kinase, p38 MAPK and extracellular signal-regulated kinase-1/2. | |||||||||||||||
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Acetaldehyde can also induce apoptosis via activation of stress signaling such as c-Jun phosphorylation [34,106,107]. | |||||||||||||||
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and other transcription factors like AP-1 and NF-? | |||||||||||||||
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Upon activation, JNKs translocate to the nucleus to phosphorylate and enhance the transcriptional activity of JUN [7]. | |||||||||||||||
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ERK phosphorylates and thereby activates downstream targets like the transcription factor c-Jun. | |||||||||||||||
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Vpr activates the DNA binding activity of AP-1 by promoting the phosphorylation of cFos and cJun in monocytes and macrophages [267]. | |||||||||||||||
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It has been demonstrated that during reperfusion, oxidative stress leads to activation and translocation of JNK to the nucleus, where phosphorylation of transcription factors, such as c-Jun occurs.
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Phosphorylation of c-Jun is a prerequisite of AP-1 dimerization and activation. | |||||||||||||||
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Phosphorylation of GST-c-Jun was then determined by autoradiography.
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Phosphorylation of c-Jun is a prerequisite of AP-1 dimerization and activation. | |||||||||||||||
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General Comments
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