| Gene name: | LSD1 |
| Aging type: | Prevent |
| Aging characteristic: |
| Tissue type: | -- |
| Cell name: | PC-3 |
| Experiment: | RT-qPCR//SA-β-gal activity assay//Knockdown |
| Description: | LSD1-depleted cells underwent cellular senescence as manifested by increased expression of senescence markers, including positivity of pronounced foci for the heterochromatin marker H3K9 trimethylation (H3K9me3)6,19, senescence-associated β-galactosidase (SA-β-gal) activity and upregulation of MMP3 gene encoding a senescent cell secretory protein20.Analogous to the effect of gene knockdown, the LSD1 inhibitor pargyline11,21 also induced senescence in both LNCaP and PC-3 cells . |
| Target gene: | H3K9ME2 |
| Official symbol(s): | H3K9ME2 |
| R-AG-Target gene: | Inhibition |
| Subcategory: | Methylation |
| Target gene experiment: | CHIP//Immunocytochemistry//SA-β-gal activity assay |
| Target gene description: | LSD1 knockdown alone induced robust cellular senescence, including increased SA-β-gal activity and positivity of pronounced foci for the heterochromatin marker H3K9me3 .Chromatin immunoprecipitation (ChIP) assay showed that the level of the transcription-repressive mark H3K9me2 in SKP2 and CDC25A promoters was significantly increased after LSD1 knockdown, and the effect was almost completely reversed by restored expression of LSD1. |
| Regulatory pathway: | -- |
| R-AG-Pathway: | -- |
| Pathway experiment: | -- |
| Pathway description: | -- |
Annotation:
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