| Gene name: | SIRT6 |
| Aging type: | Prevent |
| Aging characteristic: |
| Tissue type: | -- |
| Cell name: | HepG2 |
| Experiment: | SA-β-gal activity assay |
| Description: | Inhibiting the upregulation of SIRT6 enabled TGF-β1?H2O2?HOCl to efficiently induce cellular senescence. |
| Regulatory pathway: | ERK//SMAD//P38 MAPK |
| R-AG-Pathway: | --//--//-- |
| Official symbol(s): | MAPK1//SMAD//MAKP14 |
| Pathway experiment: | SA-β-gal activity assay |
| Pathway description: | Consistent with the promoting effect of Smad and p38 MAPK pathways on the expression of SIRT6, inhibiting each of these pathways enabled TGF-β1?H2O2?HOCl to induce the cellular senescence of HCC cells. Transforming growth factor-β1?H2O2?HOCl could induce sustained and enhanced activation of the ERK pathway.Consistently, TGF-β1?H2O2?HOCl could efficiently induce cellular senescence, if the ERK pathway was inhibited. In this situation, the effect of TGF-b1?H2O2?HOCl on cellular senescence was also attenuated by inhibiting the NF-jB,Smad, and p38 MAPK pathways, which was consistent with the effect of suppressing the upregulation of SIRT6. However, if SIRT6 expression was suppressed by shRNA, TGF-β1?H2O2?HOCl could similarly induce cellularsenescence, even though the ERK pathway was activated . |
Annotation:
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