| Gene name: | RSL1D1 |
| Aging type: | Prevent |
| Aging characteristic: | Others |
| Tissue type: | -- |
| Cell name: | HEK293,2BS |
| Experiment: | Western blot//Flow cytometry//Knockdown//SA-β-gal activity assay |
| Description: | p27Kip1 and PTEN protein levels were greatly decreased (4-fold for PTEN and 7-fold for p27Kip1) in cells with CSIG overexpression.As expected, silencing of CSIG in HEK 293 cells led to increased G0/G1 and reduced S compartments，cells overexpressing CSIG exhibited markedly elevated proliferation rates, showed increased S and reduced G1 compartments, and displayed a feature of young cells (lower SA-β-gal activity) compared with the empty-vector-transfected cells. |
| Regulatory pathway: | PTEN-P27 |
| R-AG-Pathway: | Downregulation |
| Official symbol(s): | PTEN-CDKN1B |
| Pathway experiment: | Knockdown//Western blot//qRT-PCR//RNA-binding protein (RBP) prediction analysis |
| Pathway description: | Knockdown of PTEN in HEK 293 cells greatly diminished the effect of either overexpression or knockdown of CSIG on p27Kip1 expression.To our surprise, neither overexpression nor silencing of CSIG significantly affected the mRNA levels of PTEN although the PTEN protein level was decreased by 10-fold in CSIG overexpression and increased in CSIG silenced cells (4-fold for 20 nM siRNA and 10-fold for 50 nM siRNA) by Western blot analysis.By Western blotting of CSIG in the pulldown materials, PTEN 5 UTR and CR (but not 3 UTR) were targets of CSIG. |
Annotation:
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