Gene name: | CST1 |
Aging type: | Prevent |
Aging characteristic: |
Tissue type: | -- |
Cell name: | MDA-MB-231,SW480 |
Experiment: | Knockdown//SA-β-gal activity assay//RT- PCR//Western blot |
Description: | Following CST1 knockdown, cell populations exhibiting SA-β-gal-positive staining increased to 70–80% and 55–90% in MDA-MB-231 and SW480 cells, respectively. Notably, the gene expression of representative SASP genes, including interleukin-6 (IL-6) and chemokine C-C motif ligand 20 (CCL20), was induced by CST1 knockdown in MDA-MB-231 and SW480 cells.To confirm that the G0/G1-phase cell cycle arrest was caused by CST1 knockdown, we conducted western blotting and found that CST1 knockdown suppressed cyclin D1 and phospho-retinoblastoma (p-Rb) and induced p21. |
Target gene: | CATB |
Official symbol(s): | CATB |
R-AG-Target gene: | -- |
Subcategory: | Unclear |
Target gene experiment: | Knockdown//SA-β-gal activity assay//Western blot |
Target gene description: | CST3 knockdown rescued extracellular CatB activity and significantly inhibited SA-β-gal activity in CST1 knockdown MDA-MB-231 cells.We found that CST1 knockdown suppressed extracellular, but not intracellular, CatB activity. |
Regulatory pathway: | GSK3β |
R-AG-Pathway: | -- |
Official symbol(s): | GSK3B |
Pathway experiment: | Knockdown//SA-β-gal activity assay//Western blot |
Pathway description: | The increased GSK3β phosphorylation caused by CST1 knockdown was inhibited by the addition of rCys-SN. Although SA-β-gal activity induced by CST1 knockdown was unaltered in mock vector and wild-type GSK3β-expressing cells, the ectopic expression of GSK3β-S9A (Activate form) significantly suppressed the SA-β-gal activity induced by CST1 knockdown . CatB knockdown also induced the inhibitory phosphorylation of GSK3β at serine 9. |
Annotation:
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