| Gene name: | GDF15 |
| Aging type: | Accelerate |
| Aging characteristic: |
| Tissue type: | -- |
| Cell name: | Aortic endothelial cell |
| Gene ID: | 9518 |
| Category: | protein coding |
| Phenotype: | Atherosclerosis |
| Experimental category: | HL |
| PMID: | 26909594 |
| Experiment: | SA-β-gal activity assay |
| Description: | Upregulation of GDF15 caused a decrease in cell proliferation and an increase in SA-β-gal staining compared with the control lentivirus-transduced cells. |
| Target gene: | ERK |
| Official symbol(s): | ERK |
| R-AG-Target gene: | Activation |
| Subcategory: | Unclear |
| Target gene experiment: | Western blot//Immunostaining |
| Target gene description: | We noted that ERK phosphorylation was increased following the rhGDF15 protein treatment. In addition, IR-induced ERK activation was controlled by the downregulation of GDF15.ROS generation was increased in GDF15-tranduced cells compared to control virus-transduced cells. |
| Regulatory pathway: | P16-RB |
| R-AG-Pathway: | Upregulation |
| Pathway experiment: | SA-β-gal activity assay//Cell counting//Knockdown//Western blot |
| Pathway description: | On the contrary, the overexpression of GDF15 had no significant effects on cell proliferation in the p16 knockdown cells . The measurement of SA-β-gal activity indicated that p16 knockdown inhibited GDF15-induced cellular senescence, but p53 knockdown did not.Increased expression of GDF15 induced p16 expression and treatment with GDF15 recombinant protein increased p16 mRNA by approximately 2.5 fold. Both endogenous and exogenous GDF15 protein increased p16 protein and decreased the phosphorylation of Rb, which causes its detachment from E2F transcription factor. |
Annotation:
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