INT145695
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
These observations suggest that the steady state levels of JNK1 are controlled by factors other than transcription. | |||||||||||||||
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A number of proteins negatively regulate JNK. | |||||||||||||||
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The polymorphic nature of the mitogen activated protein kinase 8 (Mapk8) gene | |||||||||||||||
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Using spinal nerve ligation to create a model of neuropathic pain, Zhuang et al. demonstrated that the up-regulation of JNK1 occurred primarily in spinal astrocytes, and that the spinal administration of a selective JNK1 inhibitor blocked the resulting hypersensitivity [21]. | |||||||||||||||
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The polymorphic nature of the mitogen activated protein kinase 8 (Mapk8) gene | |||||||||||||||
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This elevated expression was abrogated by JNK1 mutation and the JNK inhibitor, indicating the dependence of MUC5AC expression on JNK activity. | |||||||||||||||
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Cytokines administration did not alter ERK1/2 and JNK1/2 phosphorylation. | |||||||||||||||
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B, and JNK pathways are critical regulators for the production of the cytokines associated with tumor promotion. | |||||||||||||||
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B and JNK pathways are critical regulators for the production of the cytokines associated with tumor promotion.
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Then we tested the effects of JNK or p38 inhibitor on the induction of cingulate LTP, because the MAPK signaling pathways include extracellular signal-regulated (ERK), c-Jun N-terminal kinase (JNK), p38 and ERK5 [17]. | |||||||||||||||
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Then we tested the effects of JNK or p38 inhibitor on the induction of cingulate LTP, because the MAPK signaling pathways include extracellular signal-regulated (ERK), c-Jun N-terminal kinase (JNK), p38 and ERK5 [17]. | |||||||||||||||
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Then we tested the effects of JNK or p38 inhibitor on the induction of cingulate LTP, because the MAPK signaling pathways include extracellular signal-regulated (ERK), c-Jun N-terminal kinase (JNK), p38 and ERK5 [17]. | |||||||||||||||
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have been shown to regulate JNK and p38 MAPK signaling to promote apoptosis [53]. | |||||||||||||||
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There is also participation in the transcriptional regulation of growth factors such as EGF through JNK activation [61]. | |||||||||||||||
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However, the activities of other protein kinases in the MAPK pathway, including p38 and JNK, showed no changes in FrA, Acb and CPu of the mice during the chronic morphine dependence and withdrawal phases. | |||||||||||||||
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This study suggests that JNK is a potential target for prostate cancer growth. | |||||||||||||||
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Protandim diet alone did not affect either Jun D/Fra-1 or pJNK level significantly.
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We found that LPS significantly increased the concentrations of TLR-4, NF-kappaB and MAPKs, including extracellular regulated kinase (ERK), c-jun N-terminal kinase (JNK) and p38 MAPK, in activated macrophages. | |||||||||||||||
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We found that LPS significantly increased the concentrations of TLR-4, NF-kappaB and MAPKs, including extracellular regulated kinase (ERK), c-jun N-terminal kinase (JNK) and p38 MAPK, in activated macrophages. | |||||||||||||||
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There are several reports indicating that factors other than those within the IGF-1/insulin/PI3K/Akt signaling pathway are involved in the regulation of FOXO activity, including but not limited to serum and glucocorticoid-inducible kinase (SGK), jun-N-terminal kinase (JNK), and ? | |||||||||||||||
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