INT173647
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
In the decomposition of the interaction map, FOS appears in Module 2 only and MAPK14 catalyzes the activation of FOS. | |||||||||||||||
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Results showed a high expression of p38 MAPK (ATF-2) at 4 ? | |||||||||||||||
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Currently, novel p38? | |||||||||||||||
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Development of bioavailable, central nervous system-penetrant p38? | |||||||||||||||
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Oral administration of a CNS-penetrant p38? | |||||||||||||||
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The MAPK family, comprising of ERKs, JNK, and p38, is activated in response to the various stress stimuli caused by virus infections or chemical exposures. | |||||||||||||||
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However, in contrast to JNK, no significant differences in ERK1/2 (Fig. 6C, D, H) or p38 (Fig. 6E, F, I) activities were found between the specimen treated with nicotine (10 ? | |||||||||||||||
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Inhibition of the individual MAP kinase pathways with specific chemical inhibitors either completely abolished or significantly reduced expression levels of cartilage-specific genes in a pattern distinct to each pathway, thus indicating that p38, ERK, and JNK are independently essential for the TGF-? | |||||||||||||||
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Inhibition of the individual MAP kinase pathways with specific chemical inhibitors either completely abolished or significantly reduced expression levels of cartilage-specific genes in a pattern distinct to each pathway, thus indicating that p38, ERK, and JNK are independently essential for the TGF-? | |||||||||||||||
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I/R increased the expression of all three MAPKs, with significantly greater expression of JNK and p38. | |||||||||||||||
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plus epinephrine effect on IL-6, IL-8, and IL-13 expression suggesting that p38 plays an important role in signaling from both IL-1? | |||||||||||||||
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The stress-activated protein kinase/ Jun-terminal kinase SAPK/JNK, a mediator of apoptosis, was activated (phosphorylated) 16 h after treatment with either of the Sulindac metabolites (not shown), and increased further after 24 h and 48 h (Fig. 6). | |||||||||||||||
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The stress-activated protein kinase/ Jun-terminal kinase SAPK/JNK, a mediator of apoptosis, was activated (phosphorylated) 16 h after treatment with either of the Sulindac metabolites (not shown), and increased further after 24 h and 48 h (Fig. 6). | |||||||||||||||
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The stress-activated protein kinase/ Jun-terminal kinase SAPK/JNK, a mediator of apoptosis, was activated (phosphorylated) 16 h after treatment with either of the Sulindac metabolites (not shown), and increased further after 24 h and 48 h (Fig. 6). | |||||||||||||||
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Apoptosis was associated with activation of both c-Jun N-terminal protein kinase and p38 kinase and overexpression of proapoptotic proteins and cyclooxygenase 2 (COX-2) [77, 83]. | |||||||||||||||
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Apoptosis was associated with activation of both c-Jun N-terminal protein kinase and p38 kinase and overexpression of proapoptotic proteins and cyclooxygenase 2 (COX-2) [77, 83]. | |||||||||||||||
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General Comments
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