| Gene name: | SIX1 |
| Aging type: | Prevent |
| Aging characteristic: |
| Tissue type: | -- |
| Cell name: | IMR-90 |
| Experiment: | SA-β-gal activity assay//Cell morphological analysis//BrdU assay//Western blot |
| Description: | Stable silencing of SIX1 in early passage IMR90 cells markedly reduced proliferation, as assessed by bromodeoxyuridine incorporation.Most importantly, IMR90 shSIX1 cells displayed features of cellular senescence, including senescent morphology with extended vacuolized cytoplasms and prominent nucleoli, and increased number of senescence-associated β-galactosidase-positive cells. |
| Target gene: | P16//POLYCOMB |
| Official symbol(s): | P16//POLYCOMB |
| R-AG-Target gene: | --//-- |
| Subcategory: | Unclear |
| Target gene experiment: | Western blot//Immunofluorescence//qPCR//CHIP |
| Target gene description: | In agreement with the inverse correlation between SIX1 and p16 found in ER:Ras induced senescence, we observed that p16 protein and RNA levels were significantly increased in shSIX1-IMR90 cells, as did the number of p16-positive cells in immunofluorescence assays.To test if SIX1 could cooperate with Polycomb complexes in senescence, we analyzed changes in the Polycomb-associated mark H3K27Me3. ChIP showed a clear reduction of H3K27Me3 in the INK4A promoter (~5-fold) in shSIX1-senescent cells , in the absence of gross changes in the H3K27Me3 nuclear level or distribution, similar to other senescence stimuli. |
| Regulatory pathway: | -- |
| R-AG-Pathway: | -- |
| Pathway experiment: | -- |
| Pathway description: | -- |
Annotation:
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