| Gene name: | ING1 |
| Aging type: | Accelerate |
| Aging characteristic: |
| Tissue type: | -- |
| Cell name: | IMR-90 |
| Experiment: | Western blot//BrdU assay//SA-β-gal activity assay//Cell morphological analysis |
| Description: | Enforced expression of ING1 caused a dramatic reduction in proliferation, as shown by a decrease in thymidine incorporation or in the number of BrdU-positive cells.The inverse correlation between ING1 expression and BrdU incorporation could also be observed in individual cells by immunofluorescence. Eighty-five percent of AU5-positive cells were BrdU-negative, while 65% of AU5-negative cells or vector-infected cells were BrdU-negative, confirming the antiproliferative effect of ectopic ING1.ING1-expressing fibroblasts also displayed distinctive markers of cellular senescence,such as SA-Beta Gal activity , and flat enlarged morphology. |
| Regulatory pathway: | P53 |
| R-AG-Pathway: | -- |
| Official symbol(s): | TP53 |
| Pathway experiment: | Western blot//SA-β-gal activity assay |
| Pathway description: | To investigate the functional connection between p33ING1 and p53 in the context of senescence, we inactivated the p53 pathway in these cells, using the E6 oncoprotein from human papilloma virus. Ectopic expression of p33ING1 failed to induce a significant cell-cycle arrest in fibroblasts expressing E6 .Similarly, the induction of the senescence marker SA-β-Gal by p33ING1 was largely abolished in E6-expressing cells. In agreement with previous reports, inactivation of the p53 pathway was not sufficient to bypass senescence by RasV12 in these cells, which requires additional inactivation of the Rb pathway. Interestingly, ING1 increased the level of p21CIP1, a p53 target associated with senescence. The induction of p21CIP1 by ING1 was lost in E6-expressing cells . |
Annotation:
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