| Gene name: | YAP1 |
| Aging type: | Prevent |
| Aging characteristic: |
| Tissue type: | -- |
| Cell name: | MSC |
| Gene ID: | 10413 |
| Category: | protein coding |
| Phenotype: | Osteoarthritis |
| Experimental category: | HL |
| PMID: | 30933975 |
| Experiment: | SA-β-gal activity assay//Flow cytometry//Western blot |
| Description: | Phenotypic characterizations revealed that the downregulation of YAP in hMSCs also resulted in a similar premature aging phenotype. By contrast, ectopic expression of YAP rescued the premature senescence observed in YAP?/?hMSCs, as evidenced by the reduced number of SA-β-gal–positive cells ,enhanced growth rate and clonal expansion ability , decreased expression of P16 and P21, lower levels of ROS , and slower in vivo decay after engraftment. |
| Regulatory pathway: | YAP-TEAD//YAP-FOXD1 |
| R-AG-Pathway: | --//-- |
| Official symbol(s): | YAP1-TEAD//YAP1-FOXD1 |
| Pathway experiment: | SA-β-gal activity assay//Dual-Luciferase reporter assay//Western blot//Clonal expansion assay |
| Pathway description: | Similar to YAP-deficient hMSCs, TEADs KD/KO hMSCs also showed major phenotypes of premature senescence, such as an increased number of SA-β-gal–positive cells, compromised clonale. Moreover, the activity of 8 × GTIIC-Luc, a YAP/TAZ-responsive reporter, decreased in both RS hMSCs and WS hMSCs . Lentiviral overexpression of YAP or FOXD1 effectively attenuated the senescent features of RS hMSCs and WS hMSCs. |
Annotation:
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