| Gene name: | YPEL3 |
| Aging type: | Accelerate |
| Aging characteristic: |
| Tissue type: | -- |
| Cell name: | MCF-7,U2OS |
| Experiment: | Colony formation assay//SA-β-gal activity assay |
| Description: | Using a colony formation assay,both cell lines showed considerably fewer colonies when expressing YPEL3 compared with cells not induced to express YPEL3. Growth suppression was also observed after shorter time periods of YPEL3 induction. Due to difficulties in the long-term growth of YPEL3 expressing cells, the inability to detect apoptosis, and observed morphologic changes, we examined the possibility that induction of YPEL3 would trigger cellular senescence.Two hallmarks of cellular senescence in human cells are the detection of increased acidic β-galactosidase activity and the appearance of foci within the nuclei of senescent cells . A clear increase (～38%) in cellular senescence was observed in U2OS/YPEL3-TetR cells exposed to tetracycline. |
| Target gene: | P53 |
| Official symbol(s): | P53 |
| R-AG-Target gene: | -- |
| Subcategory: | Unclear |
| Target gene experiment: | Dual-Luciferase reporter assay//Immunoblotting |
| Target gene description: | The level of YPEL3 mRNA induction was significantly reduced in doxorubicintreated Hct116 cells lacking p53 .Cotransfection of the YPEL3-luciferase reporter with wild-type p53 in either Hct116?/?p53 or H1299 cells led to an increase in YPEL3 promoter activity .Having established that the YPEL3 promoter could be activated by p53 when cloned into a plasmid reporter construct, we next set out to test whether p53 protein associated with the YPEL3 promoter in vivo. p53 chromatin immunoprecipitation assays were performed with Hct116 cells undamaged (non-treated) or damaged with doxorubicin. As expected, p53 was shown to bindin vivoto the YPEL3 promoter in DNA-damaged Hct116 cells. |
| Regulatory pathway: | -- |
| R-AG-Pathway: | -- |
| Pathway experiment: | -- |
| Pathway description: | -- |
Annotation:
Loading,please wait...