| Gene name: | YAP1 |
| Aging type: | Prevent |
| Aging characteristic: | Others |
| Tissue type: | -- |
| Cell name: | IMR-90 |
| Experiment: | Knockdown//SA-β-gal activity assay//BrdU assay//Flow cytometry |
| Description: | Compared with the control, silencing YAP significantly induced cellular senescence. SA-β-gal staining and BrdUrd incorporation were used as readouts for senescence. Knockdown of YAP increases the expression of SA-β-gal and inhibits cell DNA replication.Furthermore, YAP downregulation also resulted in the inhibition of cell proliferation in a population doubling assay.As expected, YAP knockdown significantly reduced the S-phase and increased the G1-phase in the IMR90 cells. |
| Target gene: | CDK6 |
| Official symbol(s): | CDK6 |
| R-AG-Target gene: | -- |
| Subcategory: | Unclear |
| Target gene experiment: | qRT-PCR//Western blot//CHIP//Knockdown//SA-β-gal activity assay |
| Target gene description: | In our experiments, YAP or TEAD knockdown significantly inhibited CDK6 mRNA level and protein expression in IMR90 cells.Further ChIP experiments confirmed the binding NA NA of YAP to these 2 sites, whereas we used the already identified YAP–TEAD target CTGF as a positive control. Furthermore, overexpression of CDK6 can partially rescue the increased senescence induced by YAP knockdown. |
| Regulatory pathway: | TEAD//RB-P53-P16 |
| R-AG-Pathway: | --//-- |
| Official symbol(s): | TEAD//RB1-TP53-CDKN2A |
| Pathway experiment: | Knockdown//SA-β-gal activity assay//BrdU assay//qRT-PCR |
| Pathway description: | We found that knockdown of TEAD1/3/4 also induces an almost identical cellular senescent phenotype as YAP silencing. Further solidifying our hypothesis that YAP regulates cellular senescence in a TEAD-dependent manner, we found that the knockdown of boIn our SA-β-gal staining experiments, silencing either p16 or p53 did not rescue the senescent phenotype caused by YAP knockdown th YAP and We also found that the individual knockdown of p53 or p16 could not rescue the YAP knockdown-induced senescent phenotype by conducting population doubling assay experiments. However, double knockdown of p53 and p16 partially rescued YAP knockdown-induced senescence , suggesting that YAP antagonized senescence through both the p53 and p16 pathways TEAD1/3/4 together did not lead to a further increased senescent phenotype, including SA-β-gal staining and BrdUrd incorporation as well as PDL. |
Annotation:
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