| Gene name: | IFNG |
| Aging type: | Accelerate |
| Aging characteristic: |
| Tissue type: | -- |
| Cell name: | HUVEC |
| Experiment: | MTT assay//Flow cytometry//SA-β-gal activity assay |
| Description: | Cell proliferation decreased slightly with IFN-γ treatment in time- and dose-dependent manners. A decrease in cell proliferation by IFN-γ treatment for 3 days was statistically significant (p < 0.05). The induction of cellular senescence by prolonged treatment with IFN-γ was confirmed by an increase in SA-β-gal-positive cells in the treated cells compared to the control cells . IFN-γ treatment increased the G0/G1 cell population and decreased the S and G2/M cell population, suggesting that IFN-γinhibited cell proliferation through G0/G1 arrest in the cell cycle. |
| Target gene: | P53 |
| Official symbol(s): | P53 |
| R-AG-Target gene: | -- |
| Subcategory: | Unclear |
| Target gene experiment: | Knockdown//SA-β-gal activity assay//Western blot |
| Target gene description: | Prolonged stimulation of IFN-γ in the p16-knockdown (p16sh) cells increased SA-β-gal activity staining to a level similar to that in control cells. In contrast, no increase in SA-β-gal staining was observed in the p53-knockdown (p53sh) cells following prolonged stimulation with IFN-γ. We reproducibly noticed an increase in the number of SA-β-gal-positive cells in p16-/-MEFs, but not in IFN-γ-treated p53-/-MEFs, after prolonged stimulation with IFN-γ. Therefore,these results suggest that IFN-γ-induced cellular senescence is mediated through a p53-dependent pathway.To confirm that p53 activation by IFN-γ treatment was mediated through DNA damage signaling,the ATM level was down-regulated using siRNAs against ATM,followed by treatment with IFN-γ for 6 days. Increases in p53 and phospho-p53 levels induced by IFN-γ treatment were repressed by knockdown of ATM. |
| Regulatory pathway: | -- |
| R-AG-Pathway: | -- |
| Pathway experiment: | -- |
| Pathway description: | -- |
Annotation:
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