| External factors: | Nucleus accumbens-1 |
| Aging type: | Prevent |
| Aging characteristic: |
| Category: | Other |
| Phenotype: | Aging |
| Experiment: | SA-β-gal activity assay//BrdU assay/Knockdown//Western blot//Flow cytometry |
| Description: | We observed that during activation of this NAC1 deletion mutant, the cells showed a decreased proliferation rate upon continuous passaging as compared with the cells without activation of this NAC1-dominant negative mutant. We further found that the decreased proliferation was accompanied by increases in the numbers of SA-β-gal–positive cells and in the numbers of cells with altered cellular morphology such as flattening and enlargement.p21, a cyclin-dependent kinase inhibitor and an inducer of cellular senescence,was also increased. Inactivation of NAC1 also significantly enhanced the proliferation-inhibitory and the colony formation–inhibitory effects, and caused a G2–M cellcycle arrest, suggesting that senescence occurs in G2–M phase. |
| Target gene: | NP63 |
| R-EF-Target gene: | -- |
| Official symbol(s): | NP63 |
| Target gene experiment: | Knockdown//Western blot//SA-β-gal activity assay |
| Target gene description: | We found that the expression of DNp63 protein was markedly downregulated in cells with deficiency of NAC1 after treatment with g-irradiation ,The role of DNp63 in NAC1-mediated evasion of senescence was further verified by overexpressing DNp63 in NAC1-deficient cells.Ectopic expression of DNp63 in SKOV3/N130 or HeLa/N130 cells with inactivation of NAC1 or in A2780 cells with silencing of NAC1 significantly blunted the activation of senescence caused by g-irradiation. |
| Regulatory pathway: | -- |
| R-EF-Pathway: | -- |
| Pathway experiment: | -- |
| Pathway description: | -- |
Annotation: