| Gene name: | CSNK2A1 |
| Aging type: | Prevent |
| Aging characteristic: | Others |
| Tissue type: | Liver and Testis |
| Cell name: | IMR-90 |
| Experiment: | SA-β-gal activity assay |
| Description: | These reindicate that CKII activity decreases in IMR-90 cells during both replicative and H2O2-induced senescence.SA-β-gal staining in cells tended to be an increase in a dose-dependent manner by treatment with DRB.33 PDL of IMR-90 cells transfected with anti-CKIIa siRNA exhibited a higher rate of SA-β-gal staining comparedwith control cells. The increase rate in SA-β-gal staining from control was approximately 15-fold for CKIIa siRNA. |
| Target gene: | P53//P21 |
| Official symbol(s): | P53//P21 |
| R-AG-Target gene: | Activation//Activation |
| Subcategory: | Unclear |
| Target gene experiment: | Western blot |
| Target gene description: | When the protein levels of p53 and p21Waf-1 were determined by immunoblot, expression of both proteins was upregulated in CKII inhibitor-treated cells, like in H2O2- induced senescent cells.We examined if these CKII inhibitor-treated cells would display other senescent characteristics. The activation of p53 and p21Waf-1 is essential for cells to establish and maintain cellular senescence [24, 28]. Therefore, we examined whether p53 and p21Waf-1 would be overexpressed in IMR-90 cells treated with CKII inhibitors. When the protein levels of p53 and p21Waf-1 were determined by immuno-blot, expression of both proteins was upregulated in CKII inhibitor-treated cells, like in H2O2-induced senescent cells (Fig. 4D). Taken together, these results indicate that inhibition of CKII activity by exogenously added CKII inhibitors can induce premature senescence of IMR-90 cells. |
| Regulatory pathway: | -- |
| R-AG-Pathway: | -- |
| Pathway experiment: | -- |
| Pathway description: | -- |
Annotation:
Loading,please wait...