| Gene name: | PTEN |
| Aging type: | Accelerate |
| Aging characteristic: |
| Tissue type: | Human islet |
| Cell name: | -- |
| Experiment: | Knockdown//Immunostaining |
| Description: | The percentage of Ki67 positive cells was dramatically increased in the Pten null mice that are 3 months old and older. |
| Regulatory pathway: | PI3K-AKT//CYCLIN D1-E2F-EZH2-P16 |
| R-AG-Pathway: | Downregulation//-- |
| Official symbol(s): | PIK3CA-AKT1//CCND1-E2F1-EZH2-CDKN2A |
| Pathway experiment: | Western blot |
| Pathway description: | A primary biochemical function of PTEN is to inhibit the action of PI3K.We show that phosphorylation of the PI3K effector, serine/threonine kinase AKT, is dramatically induced in the Pten null islets compared with the Con ones, whereas the amount of p-ERK is minimally altered.Elevated cyclin D1 leads to the activation of E2F through phosphorylation of retinoblastoma (RB) proteins. We found that overexpression of E2F1 led to downregulation of p16ink4a expression, whereas knockdown of E2F1 robustly induced expression of p16ink4a.We found that expression of E2Fs1-4,especially E2Fs1-3, resulted in the dramatic induction of an Ezh2 promoter activity. |
Annotation:
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