| Gene name: | RAF1 |
| Aging type: | Accelerate |
| Aging characteristic: | Others |
| Tissue type: | -- |
| Cell name: | IMR-90 |
| Experiment: | Cell counting//SA-β-gal activity assay |
| Description: | Activation of GFPDRaf-1:ER arrested the proliferation of IMR-90 cells.Activation of GFPDRaf-1[YY]:ER in IMR-90 cells elicited the expression of acidic β-galactosidase, which was apparent within 2 3 days and maximal by 5 6 days after addition of 4-HT. |
| Target gene: | P16 |
| Official symbol(s): | P16 |
| R-AG-Target gene: | Upregulation |
| Subcategory: | Unclear |
| Target gene experiment: | Western blot//SA-β-gal activity assay//BrdU assay//Flow cytometry |
| Target gene description: | Following activation of GFPDRaf-1:ER, we observed induced expression of the CDK inhibitors p16Ink4a.However, the level of expression of p16Ink4a did not decrease after GFPDRaf-1:ER inactivation, which may reflect the long half-life of both p16Ink4a mRNA and protein.IMR-90 cells expressing p16Ink4a became positive for SA–β-galactosidase activity.FACs can analysis revealed a threefold reduction in S-phase cells compared with the control infected populations. |
| Regulatory pathway: | MEK-MAPK |
| R-AG-Pathway: | Activation |
| Official symbol(s): | MAP2K7-MAPK1 |
| Pathway experiment: | Western blot |
| Pathway description: | As described above, activation of GFPDRaf-1[YY]:ER led to the phosphorylation and activation of the p42/p44 MAP kinases. In the presence of PD, however, phosphorylation of the MAP kinases was reduced to levels comparable to those found in uninduced IMR-90 cells. |
Annotation:
Loading,please wait...