| Gene name: | CSNK2A1 |
| Aging type: | Prevent |
| Aging characteristic: |
| Tissue type: | -- |
| Cell name: | HCT116 |
| Experiment: | SA-β-gal activity assay//Knockdown |
| Description: | Transfection of CKII a siRNA markedly increased SA- β-gal staining, whereas rapamycin, vitamin C, and vitamin E treatment suppressed SA- β-gal staining . |
| Regulatory pathway: | PI3K-AKT-MTOR-ROS |
| R-AG-Pathway: | -- |
| Official symbol(s): | PIK3CA-AKT1-MTOR-ROS1 |
| Pathway experiment: | Western blot//Flow cytometry//SA-β-gal activity assay |
| Pathway description: | We found that triciribine reduced the rate of CKII inhibition induced senescence.Consistent with this, we observed that triciribine completely abolished CKII downregulation induced overexpression of p53 and p21 Cip1/WAF1.In addition, triciribine reduced phosphorylation of mTOR (S2448) and AKT (S473), suggesting that AKT acts as a positive regulator of mTOR in cells made senescent by CKII inhibition. Furthermore, overexpression of CKII a clearly suppressed phosphorylat ion of AKT (473) as well as mTOR (2448) . Finally, incubation with triciribine reduced production of hydrogen peroxide and superoxide anion in CKII a-downregulated cells. co-treatment of cells with wortmannin dramaticall y reduced the rate of SA- β-gal staining . Whereas p53 and p21 Cip1/WAF1 expression levels were elevated in DRB-treated cells compared with to control cells, wortmannin apparentl y downregulated the expression of these proteins.Consistent with this, wortmannin almost completely blocked activation of p53 and p21 Cip1/WAF1 in cells transfected with CKIIa siRNA wortmannin attenuated phosphorylation of mTOR (S2448), p70S6K, and AKT (S473), suggesting that PI3K acted as a positive regulator of mTOR in cells made senescent by CKII inhibition. CKII a knockdown significantly increased hydrogen peroxide and superoxide anion levels relative to control cells, as indicated by green and red fluorescence.incubation with wortmannin apparently prevented green and red fluorescence in CKII adownregulated cells.wortmannin had no effect on the catalytic activity of CKII in cells, indicating that CKII is an upstream regulator of PI3K .Western blot analysis revealed that overexpression of CKII a reduced phosphorylation of both mTOR (2448) and p70S6K by 60% compared to control cells.DRB significantly increased hydrogen peroxide and superoxide anion levels relative to untreated control cells, as indicated by green and red fluorescence. However, incubation with rapamycin, vitamin C, and vitamin E apparently prevented both fluorescent signals in DRB-treated cells. Vitamin C and vitamin E are well known ROS scavenger s, whereas rapamyci n is an mTOR inhibitor. |
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