Gene name: | IFNG |
Aging type: | Accelerate |
Aging characteristic: | Others |
Tissue type: | -- |
Cell name: | HUVEC,MEF |
Gene ID: | 3458 |
Category: | protein coding |
Phenotype: | Atherosclerosis |
Experimental category: | L |
PMID: | 19071156 |
Experiment: | Cell proliferation assay//Flow cytometry//SA-β-gal activity assay |
Description: | Cell proliferation decreased slightly with IFN-g treatment in time- and dose-dependent manners. A decrease in cell proliferation by IFN-g treatment (more than 1000 U/ml) for 3 days was statistically significant (p < 0.05).The induction of cellular senescence by prolonged treatment with IFN-g was confirmed by an increase in SA-β-gal-positive cells in the treated cells compared to the control cell. IFN-γ treatment increased the G0/G1 cell population and decreased the S and G2/M cell population, suggesting that IFN-γ inhibited cell proliferation through G0/G1 arrest in the cell cycle. No difference in cell cycle status was observed in IFN-a treated cells for 6 days. |
Regulatory pathway: | P53 |
R-AG-Pathway: | -- |
Official symbol(s): | TP53 |
Pathway experiment: | Knockdown//Western blot//SA-β-gal activity assay |
Pathway description: | Prolonged stimulation of IFN-g 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-g. To obtain more evidence that IFN-g-induced senescence involves a p53 signaling pathway, we measured the effects of IFN-g on cellular senescence in wild, p16-/-, or p53-/- MEFs. We reproducibly noticed an increase in the number of SA-b-galpositive cells in p16-/- MEFs, but not in IFN-g-treated p53-/- MEFs, after prolonged stimulation with IFN-g. Therefore, these results suggest that IFN-g-induced cellular senescence is mediated through a p53-dependent pathway. |
Annotation:
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