| Gene name: | SMC1A |
| Aging type: | Prevent |
| Aging characteristic: |
| Tissue type: | -- |
| Cell name: | IMR-90 |
| Experiment: | SA-β-gal activity assay//Cell morphological analysis//Flow cytometry//Knockdown |
| Description: | We found that knockdown of either genes resulted in significant increase of SA-βgal positive cells (p< 0.0001 for all cultures) when compared to EV (EV = 9.6% SD 1.9, shB2= 55.4 SD 7.1, shS2= 74.7% SD 2.86, SEN= 80.2% SD 3.42). Cells depleted of either gene also underwent drastic changes in morphology reminiscent of SEN, such as larger size and flatter morphology.When analyzed by FACS for a senescent-like phenotype (i.e. elevated size and/or AF), we observed significantly higher number of cells bearing senescent-like features in BUB1 and SMC1A-depleted cultures relative to EV (shB2: p=0.0013; shS2: p<0.0001), similar to what observed in SEN cultures. |
| Regulatory pathway: | CDKN2A-RB1//TP53-CDKN1A |
| R-AG-Pathway: | --//-- |
| Official symbol(s): | Regulation of retinoblastoma protein//TP53-CDKN1A |
| Pathway experiment: | IF |
| Pathway description: | Cultures depleted of BUB1 and SMC1A were significantly enriched for the frequency of CDKN2A and for CDKN1A positive cells. |
Annotation:
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