| Gene name: | RXRA |
| Aging type: | Prevent |
| Aging characteristic: |
| Tissue type: | -- |
| Cell name: | MRC-5 |
| Experiment: | Knockdown//SA-β-Gal activity assay |
| Description: | RXRA knockdown decreased cell proliferation as we observed a drop in the expression of the cell proliferation marker Ki‐67 and a decrease in the number of cells .Importantly, RXRA knockdown also caused an increased SA‐β‐galactosidase activity. |
| Target gene: | P53 |
| Official symbol(s): | P53 |
| R-AG-Target gene: | -- |
| Subcategory: | Unclear |
| Target gene experiment: | Knockdown//Western blot |
| Target gene description: | Using the same approach,we further showed that cellular senescence induced by RXRA knockdown was also dependent on MCU and p53. |
| Regulatory pathway: | ITPR2-MCU |
| R-AG-Pathway: | -- |
| Official symbol(s): | ITPR2 |
| Pathway experiment: | Knockdown//qRT-PCR//Western Blot//SA-β-Gal activity assay |
| Pathway description: | To assess whether this senescent phenotype was dependent on ITPR2, we knocked down ITPR2 together with RXRA.ITPR2 knockdown impaired the upregulation of CDKN1A and GDF15 . The proliferation arrest and the increase in SA‐β‐galactosi-dase activity triggered by RXRA knockdown were alsoimpaired. Similar observations were made using either a siITPR2 pool or individual siRNAs targeting ITPR2. Using the same approach, we further showed that cellular senescence induced by RXRA knockdown was also dependent on MCU and p53. |
Annotation:
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