External factors
| External factors: |
Montelukast |
| Category: |
Chemical compounds |
| Phenotype: |
Osteoarthritis |
| Experiment: |
SA-β-gal activity assay//Immunostaining//Flow cytometry |
| Description: |
However,treatment with the specific cysLTR1 antagonist montelukast (10 and 20μM) ameliorated TNF-α-induced elevation of SA-β-Gal activity.Treatment with TNF-α (10 ng/ml) significantly increased γ-H2AX foci formation, which was prevented by montelukast in a dose-dependent manner. However, treatment with montelukast (10 and 20 μM)reduced the proportion of cells in the G0/G1 phase to 55.6% and 52.1%, respectively. |
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Regulatory relationship
| Regulatory pathway:
|
SIRT1-p53 |
| Official symbol(s): |
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SIRT1-TP53
|
| Pathway experiment: |
IP//Western blot |
| Pathway description: |
Immunoprecipitation assay results indicate that TNF-α significantly enhanced p53 K382 acetylation, which was inhibited by montelukast.The results indicate that TNF-α significantly reduced expression of SIRT1, which was prevented by montelukast in a concentration-dependent manner.Silencing of SIRT1 blocked the inhibitory effects of montelukast on p53 K382 acetylation. |
Aging network
Annotation:
The green line represents Upregulation.
The purple line represents Downregulation.
The orange line represents Activation.
The yellow line represents Inhibition.
The gray line represents Unclear.
Related pathway view