| Gene name: | VENTX |
| Aging type: | Accelerate |
| Aging characteristic: | Others |
| Tissue type: | -- |
| Cell name: | 293,IMR-90 |
| Experiment: | SA-β-gal activity assay//Cell proliferation assay |
| Description: | Consistent with its role as an inhibitor of cell proliferation, induction of VentX expression is associated with significant inhibition of U2OS/VentXTet cell growth. Interestingly, VentX expression caused a striking morphological change with U2OS/VentXTet cells appeared to be enlarged and flattened. These cells displayed positive staining for SA β-galactosidase, a characteristic marker of cellular senescence. |
| Regulatory pathway: | P53-P21//P16-RB |
| R-AG-Pathway: | Activation//Activation |
| Official symbol(s): | TP53-CDKN1A// |
| Pathway experiment: | Western blot//CHIP//Luciferase reporter assay//RT-PCR |
| Pathway description: | We found that VentX expression led to a significant increase in the protein levels of p53 and two CDK inhibitors: p21 and p16ink4a ,Consistently, we showed that ectopic expression of VentX trans-activated the human p53 and p21 promoter-luciferase reporters in a dose-dependent manner.A ChIP assay therefore was performed to examine a potential direct interaction between VentX and the p53 promoter. The ChIP assay revealed a specific binding of VentX to the p53 promoter. The potential transcriptional activation of p16ink4a by VentX was suggested by the increased p16ink4a mRNA levels upon ectopic expression of VentX . Using p16ink4a promoterluciferase reporter assay, we further demonstrated that VentX promoted p16ink4a transactivation in a dose depend ent manner. Human p16 promoter also contains putative homeodomain binding sites.Consistently, the ChIP assay demonstrated a specific binding of VentX to the p16ink4a promoter. |
Annotation:
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