| Gene name: | PRDX3 |
| Aging type: | Prevent |
| Aging characteristic: |
| Tissue type: | -- |
| Cell name: | HTR8,Human primary trophoblast |
| Gene ID: | 10935 |
| Category: | protein coding |
| Phenotype: | Intrahepatic cholestasis of pregnancy |
| Experimental category: | HL |
| PMID: | 27958341 |
| Experiment: | ROS assay//SA-β-gal activity assay//Flow cytometry |
| Description: | As expected, knockdown of PRDX3 significantly induced mitochondrial dysfunction, as indicated by overproduction of ROS, loss of mitochondrial membrane potential and decline in ATP content .Subsequently, the cell cycle distributions of these cell strains were analysed with flow cytometer. Compared to the sh-scr cells, shPRDX3-1# and shPRDX3-2# cells exhibited prolonged G0/G1 phase, indicative of growth arrest.In our study, PRDX3-knockdown cells showed a significantly higher number of SA-β-gal stained cells compared with sh-scr control cells at basal level. |
| Target gene: | P16//P21//P38 |
| Official symbol(s): | P16//P21//P38 |
| R-AG-Target gene: | --//--//-- |
| Subcategory: | Unclear |
| Target gene experiment: | qRT-PCR//Western blot//HC assay |
| Target gene description: | QRT-PCR assay revealed that mRNA levels of p21WAF1/CIP and p16INK4A were increased in PRDX3-knockdown cells compared with sh-scr cells.Immunoblot assay also confirmed the corresponding change of protein levels of p21WAF1/CIP and p16INK4A in PRDX3-knockdown cells,and in ICP placentas by immunoblot and IHC assays.Indeed, we observed elevated p38-MAPK phosphorylation in PRDX3-knockdown cells. |
| Regulatory pathway: | -- |
| R-AG-Pathway: | -- |
| Pathway experiment: | -- |
| Pathway description: | -- |
Annotation:
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