INT150547
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
Sevoflurane exposure also induced phosphorylation of apoptosis signal-regulating kinase-1 (ASK1), MAP kinase kinases 3 and 6 (MKK3/MKK6), and ATF-2. | |||||||||||||||
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Our results indicated that although both MKK3 and MKK6 were constitutively phosphorylated in the human OA chondrocytes (probably refecting the pre-activated state), but the effect of IL-1? | |||||||||||||||
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-induced phosphorylation of both MKK3 and MKK6 in a dose dependent manner with the maximum inhibitory effect of PE being at 50 ? | |||||||||||||||
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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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Higher concentrations produced no additional suppression of phosphorylation of either MKK3 or MKK6 in human OA chondrocytes.
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Our results show that both MKK3 and MKK6 were constitutively phosphorylated in the primary human OA chondrocytes but the intensity of MKK3 phosphorylation was significantly enhanced (P < 0.05) after stimulation with IL-1? | |||||||||||||||
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Our results show that both MKK3 and MKK6 were constitutively phosphorylated in the primary human OA chondrocytes but the intensity of MKK3 phosphorylation was significantly enhanced (P < 0.05) after stimulation with IL-1? | |||||||||||||||
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We then used these antibodies to determine the expression and phosphorylation of MKK3 and MKK6 proteins in human OA chondrocytes. | |||||||||||||||
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General Comments
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