| Gene name: | NF1 |
| Aging type: | Accelerate |
| Aging characteristic: |
| Tissue type: | Mice ear |
| Cell name: | -- |
| Experiment: | SA-β-gal activity assay//Knockdown |
| Description: | Importantly, we found that deep dermal lesions derived from control Tyr::CreER T2 ; Braf CA/+ mice stained positive for senescence associated–β-galactosidase, as has been shown in human nevi and in lesions within the Braf V600E - driven mouse model described by Dhomen and colleagues . However, senescence was not observed in Tyr::CreER T2 ; Braf CA/+; Nf1 flox/flox mice. These results are consistent with our cellular studies and indicate that mutations in Nf1 prevent Braf -induced senescence of melanocytes in mice, thereby rescuing the proliferative restriction and triggering excessive proliferation. |
| Regulatory pathway: | PI3K-AKT-MTOR |
| R-AG-Pathway: | -- |
| Official symbol(s): | PIK3CA-AKT1-MTOR |
| Pathway experiment: | Western blot |
| Pathway description: | Moreover,Nf1 mutations minimized the suppressive effects of Braf mutations on this pathway.Notably, we found that the PI3K inhibitor GDC-0941 prevented melanocytic hyperplasia in Tyr::CreER T2;Braf CA/+ ; Nf1 flox/flox mice,showing that Nf1 loss was mediating its effects in melanocytes, in part, by permitting or enhancing the activation of this pathway. |
Annotation:
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