INT162368
From wiki-pain
|
|
|
|
|
Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
Accordingly, Cot/tpl2 deficiency provoked a 25-30% reduction in luminol-mediated bioluminescence and neutrophil recruitment together with a 65% lower macrophage recruitment 4 h following zymosan-induced peritonitis. | |||||||||||||||
| |||||||||||||||
|
We showed that inhibition of Tpl2 markedly reduced IL-1? | |||||||||||||||
| |||||||||||||||
|
This review will describe the physiological regulation and importance of Cot/Tpl-2 in inflammation as well as the landscape of small molecules that have been reported as Cot/Tpl-2 inhibitors. | |||||||||||||||
| |||||||||||||||
|
By inference, pharmaceutical agents that inhibit Cot/Tpl-2 kinase have the potential to be novel and effective therapies for the treatment of these diseases. | |||||||||||||||
| |||||||||||||||
|
However, Tpl2 inhibition did not totally block the lipolytic effect of TNF-? | |||||||||||||||
| |||||||||||||||
|
Transfection of siRNA against Tpl2 achieved >80% efficiency in reducing endogenous Tpl2 protein levels (Fig. 4A). | |||||||||||||||
| |||||||||||||||
|
Tpl2 inhibitor acts as a potent, reversible, and ATP-competitive inhibitor of Tpl2 with an IC50 of 50 nmol/l. | |||||||||||||||
| |||||||||||||||
|
In human adipocytes, pharmacological inhibition of Tpl2 also inhibited ERK1/2 activation induced by IL-1? | |||||||||||||||
| |||||||||||||||
|
Tpl2 inhibitor acts as a potent, reversible, and ATP-competitive inhibitor of Tpl2 with an IC50 of 50 nmol/l. | |||||||||||||||
| |||||||||||||||
|
in adipocytes nearly suppressed the cytokine-induced MEK or ERK1/2 phosphorylation, whereas after inhibition of Tpl2, some phosphorylation remained. | |||||||||||||||
| |||||||||||||||
|
Tpl2 inhibition markedly blunted the effects of IL-1? | |||||||||||||||
| |||||||||||||||
|
Furthermore, compared with Tpl2 inhibitors, drugs that inhibit IKK? | |||||||||||||||
| |||||||||||||||
|
This could be because siRNA knockdown or pharmacological inhibition of Tpl2 was not sufficient to completely shutdown Tpl2 activity. | |||||||||||||||
| |||||||||||||||
|
treatment was strongly prevented when cells were pretreated with the Tpl2 inhibitor (Fig. 3D and E). | |||||||||||||||
| |||||||||||||||
|
According to this pattern one were supposed to have reduced EST, (from 3 to 2), and three of them that were supposed to report increased EST, from 4 to 5 and 6 to 7 respectively, after EA as compared with before EA.
| |||||||||||||||
| |||||||||||||||
|
Tpl2 knockdown markedly decreased MEK and ERK1/2 phosphorylation induced by IL-1? | |||||||||||||||
| |||||||||||||||
|
MEK inhibition by U0126 treatment slightly decreased basal lipolysis and inhibited cytokines effect to a level comparable to the effect observed following Tpl2 inhibition (Fig. 5A and B). siRNA-mediated silencing of Tpl2 also reduced IL-1? | |||||||||||||||
| |||||||||||||||
|
EST increase was reported by 5 (23%) of the 22 women, unchanged by 11 (50%) and a decreased EST by the remaining 6 (27%) women. | |||||||||||||||
| |||||||||||||||
|
General Comments
This test has worked.