| Gene name: | ATM |
| Aging type: | Prevent |
| Aging characteristic: |
| Tissue type: | -- |
| Cell name: | DLD1,HCT116 |
| Gene ID: | 472 |
| Category: | protein coding |
| Phenotype: | Colorectal cancer |
| Experimental category: | HL |
| PMID: | 28093285 |
| Experiment: | SA-β-gal activity assay//Knockdown//Flow cytometry |
| Description: | Intriguingly, cell cycle analysis showed that ATM deletion induced a significant G2/M arrest of DLD1 and HCT116 cells under normal conditions.Moreover, we observed a significantly higher number of senescent ATM-/- cells compared with senescent ATM+/+ cells, as determined by SA-β-gal staining . |
| Target gene: | B56γ2 |
| Official symbol(s): | PPP2R5C |
| R-AG-Target gene: | Inhibition |
| Subcategory: | Ubiquitylation |
| Target gene experiment: | Western blot//Co-IP |
| Target gene description: | Indeed,western blot analysis showed that B56γ2 expression was significantly increased in ATM-/-cancer cells.Intriguingly, the coimmunoprecipitation experiments showed that ATM and B56γ2 co-immunoprecipitated reciprocally. |
| Regulatory pathway: | CHK1-P53-P21 |
| R-AG-Pathway: | -- |
| Official symbol(s): | CHEK1-TP53-CDKN1A |
| Pathway experiment: | Western blot//Knockdown |
| Pathway description: | The results showed that in ATM-/- cells, Cdc2 phosphorylation on Tyr15, which is indicative of decreased Cdc2 activity, was significantly increased . In addition, the phosphorylation of the upstream regulator Chk1 was significantly increased in ATM-/- cells, whereas the phosphorylation of Chk2 was not altered . In accordance with this phenomenon, the phosphorylation levels of p53 and p21, two key regulators of senescence [23], were significantly increased in ATM-/-cells, indicating that ATM deficiency promotes p53/p21-induced senescence. |
Annotation:
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