| Gene name: | RPS14 |
| Aging type: | Accelerate |
| Aging characteristic: |
| Tissue type: | -- |
| Cell name: | IMR-90 |
| Experiment: | SA-β-gal activity assay//Western blot |
| Description: | Next, we characterized the effects of directly decreasing the ribosome biogenesis factors RSL1D1, NS, DDX21 or EBP2 using shRNAs. Depletion of these factors induced a proliferation arrest, a decrease in the proliferation markers KI67 and CENPA, and an increase in senescence-associated β-galactosidase staining (SA-β-gal). |
| Target gene: | CDK4//CYCLIN D1 |
| Official symbol(s): | CDK4//CYCLIN D1 |
| R-AG-Target gene: | --//-- |
| Subcategory: | Phosphorylation Unclear |
| Target gene experiment: | Pull-down assay |
| Target gene description: | GST pull down assays with purified proteins revealed that RPS14 binds to either CDK4 or cyclinD1 alone or to the complex of CDK4 with cyclinD1. |
| Regulatory pathway: | RB |
| R-AG-Pathway: | -- |
| Official symbol(s): | retinoblastoma |
| Pathway experiment: | Pull-down assay//SA-β-gal activity assay//Western blot//Knockdown |
| Pathway description: | The E7 mutant Δ79 83, which binds and inhibits Rb, rescued cells from senescence after knockdown of RSL1D1, while mutants E7Δ6 10 and E7Δ21 24 that do not bind Rb were not efficient at inhibiting senescence after knockdown of RSL1D1. Furthermore, the kinases CDK4 and CDK6, which are able to phosphorylate and inactivate Rb29, were also capable of preventing senescence after knockdown of RSL1D1. Expression of intact CDK4, but not of a catalytically inActivate mutant (CDK4(K35M)), efficiently bypassed senescence, preventing the downregulation of Ki67 expression, as well as rescuing Rb phosphorylation and the expression of E2F targets such as CENPA and MCM6 after knockdown of RSL1D1 . |
Annotation:
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