| Gene name: | AKT1 |
| Aging type: | Accelerate |
| Aging characteristic: |
| Tissue type: | -- |
| Cell name: | Human endothelial cell |
| Experiment: | SA-β-gal activity assay |
| Description: | Long-term culture studies showed that constitutive activation of Akt significantly shortened the lifespan of the endothelial cells, whereas inhibition of Akt activity delayed senescence compared with mock-infected cells ,AktCA-transduced endothelial cells were flattened and enlarged, while mock- or AktDN-infected endothelial cells exhibited normal morphology and growth.Senescence-associated b-galactosidase activity was also increased in AktCA-transduced cells. |
| Regulatory pathway: | P53-P21 |
| R-AG-Pathway: | Upregulation |
| Official symbol(s): | TP53-CDKN1A |
| Pathway experiment: | Western blot//Luciferase reporter assay |
| Pathway description: | Expression of p53 and p21Waf1/Cip1, but not p16Ink4a, was elevated, while the level of phosphorylated Rb was decreased in AktCA-infected cells compared with mock infected cells, suggesting that Akt may induce growth arrest by upregulating p53 and p21，Aktinduced cell growth arrest was restored in p21-deficient MEF, suggesting that p21 is essential for Aktinduced growth arrest of these cells.Introduction of AktCA induced p53 promoter-driven luciferase activity compared with mock infection, but not luciferase activity driven by a promoter containing 15 copies of a similar sequence with mutation at critical positions (MG15),Ablation of p53 also lessened the decrease in the lifespan of AktCA-infected cells. |
Annotation:
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