| External factors: | Coumestrol |
| Aging type: | Accelerate |
| Aging characteristic: |
| Category: | Chemical compounds |
| Phenotype: | Aging |
| Experiment: | SA-β-gal activity assay |
| Description: | SA-β-gal staining in cells tended to increase in a dose-dependent manner upon coumestrol treatment . |
| Target gene: | CKII |
| R-EF-Target gene: | Downregulation |
| Official symbol(s): | CSNK2A1 |
| Target gene experiment: | Western blot//SA-β-gal activity assay//Quantificationby densitometry |
| Target gene description: | Coumestrol decreased CKII activity in a dosedependent manner. Specifically, coumestrol treatment (20 lM) induced a 60% decrease in CKII phosphotransferase activity toward the synthetic peptide substrate. The inhibitory effect of coumestrol on CKII was also tested using dephosphorylated b-casein as a substrate. Quantificationby densitometry revealed that 10 lM coumestrol significantly inhibited CKII activity, based on a 70% decrease in b-casein phosphorylation.Transfection of these two cell types with CKIIa resulted in inhibition of SA-b-gal staining. |
| Regulatory pathway: | p53-p21 |
| R-EF-Pathway: | Activation |
| Official symbol(s): | TP53-CDKN1A |
| Pathway experiment: | Western blot |
| Pathway description: | Immunoblotting showed that the protein expression levels of p53 and p21Cip1/WAF1 were upregulated in coumestrol-treated cells.co-treatment of cells with CKIIa induced an apparent decrease in p53 and p21Waf-1 protein expression. |
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