INT86534
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
Sodium salicylate-induced apoptosis of human peripheral blood eosinophils is independent of the activation of c-Jun N-terminal kinase and p38 mitogen-activated protein kinase. | |||||||||||||||
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Secretion requires intracellular calcium mobilization and activation of phosphinositol-3 kinase and p38 mitogen activated kinase. | |||||||||||||||
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The activation of inflammation-associated enzymes such as p38 mitogen-activated protein kinase (p38 MAPK) and cycloxygenase-2 (COX-2) is not restricted to glial cells but also found in neurons and may contribute to intraneuronal damage. | |||||||||||||||
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activates p38? | |||||||||||||||
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-induced activation of p38-MAPK in human OA chondrocytes. | |||||||||||||||
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-induced activation of p38-MAPK isoforms in human OA chondrocytes. | |||||||||||||||
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-induced activation of p38? | |||||||||||||||
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was more pronounced on the phosphorylation of MKK3 as compared to MKK6 suggesting that MKK3 may be the primary kinase involved in the activation of p38-MAPK in human OA chondrocytes. | |||||||||||||||
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-induced activation of p38-MAPK in human OA chondrocytes | |||||||||||||||
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-induced activation of p38? | |||||||||||||||
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For instance, MKK6 is the major activator of p38-MAPK in cells exposed to osmotic stress [13] and MKK3 is required for full activation of p38-MAPK in murine embryonic fibroblasts [38]. | |||||||||||||||
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Our results demonstrate a novel mechanism of sulindac-induced apoptosis in human MM cells, namely, accumulation of p53, Bax, and Bak in mitochondria mediated by p38 MAPK activation downstream of ROS production. | |||||||||||||||
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It could also activate c-Jun N-terminal kinase (JNK) and p38 MAPK but not extracellular signal-regulated protein kinase (ERK) activity within 1 h. | |||||||||||||||
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The activation of inflammation-associated enzymes such as p38 mitogen-activated protein kinase (p38 MAPK) and cycloxygenase-2 (COX-2) is not restricted to glial cells but also found in neurons and may contribute to intraneuronal damage. | |||||||||||||||
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-induced activation of p38-MAPK compared to the level noted in cells with knockdown expression of MKK6. | |||||||||||||||
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-induced activation of p38-MAPK (Figure 2b, c), but the inhibition of phosphorylation was more pronounced when the expression of MKK3 was knocked down compared to the knockdown of MKK6 (Figure 2b).
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Key to these pathways are the evolutionarily conserved mitogen-activated protein kinases (MAPKs); of these, p38-MAPK (also known as MAPK14) has received considerable attention as potential therapeutic target for inflammatory and degenerative diseases such as OA [33]. p38-MAPK is thought to be crucial because selective p38-MAPK inhibitors block joint inflammation and destruction in several animal models of arthritis [12]. | |||||||||||||||
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-induced production of MMPs by blocking the activation of p38-MAPK and the transcription factor NF-? | |||||||||||||||
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Thus, treatment with PE affects particularly the activation of MKK3 which in turn has an impact on the activation of p38-MAPK downstream (summarized in Figure 6). | |||||||||||||||
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CONCLUSION: There is no direct relationship between the activation of JNK and p38 MAPK pathways and NaSal-induced apoptosis in human peripheral blood eosinophils.
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General Comments
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