| Gene name: | NRAS |
| Aging type: | Accelerate |
| Aging characteristic: |
| Tissue type: | -- |
| Cell name: | Melanocyte |
| Experiment: | Immunostaining//Cell morphological analysis//SA-β-gal activity assay//DAPI staining//SAHF |
| Description: | As expected, 15 days post-transduction the majority of N-RASQ61K transduced melanocytes displayed several markers of oncogene-driven senescence, namely cell flattening, increase in cellular size, significantly reduced Ki67 expression, increased SA-β-Gal activity and the formation of SAHF. |
| Regulatory pathway: | MAPK//AKT//P16INK4A-PRB//P53-P21WAF1 |
| R-AG-Pathway: | Activation//Activation//Activation//Activation |
| Official symbol(s): | MAPK////CDKN2A-RB1//TP53-CDKN1A |
| Pathway experiment: | Western blot |
| Pathway description: | N-RASQ61K induced melanocyte senescence was also associated with activation of the MAPK and AKT pathways, as shown by the increased phosphorylation of ERK (p-ERK), and AKT (p-AKT) at 5,10 and 15 days post infection.In addition, expression of oncogenic N-RAS led to p53 induction, increased expression of the p16INK4a and p21Waf1 cyclin dependent kinase inhibitors and reduced accumulation of pRb phosphorylated at serine residues -807 and -811 (p-pRb).These data suggest that the activation of pRb is the dominant effector of oncogene-induced melanocyte senescence. |
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