| Gene name: | SIRT6 |
| Aging type: | Prevent |
| Aging characteristic: |
| Tissue type: | -- |
| Cell name: | HBEC |
| Gene ID: | 51548 |
| Category: | protein coding |
| Phenotype: | Lung cancer |
| Experimental category: | L |
| PMID: | 24367027 |
| Experiment: | Western blot//SA-β-gal activity assay//Immunofluorescence |
| Description: | Overexpression of SIRT6 significantly suppressed HBEC senescence after CSE exposure.Intriguingly, compared with control vector, a slight decrease in HBEC senescence was observed by SIRT6 overexpression even in the absence of CSE, especially when measured by means of SA-β-gal staining. Conversely, SIRT6 knockdown increased the percentage of senescent cells, indicating that intrinsic SIRT6 is not sufficient to completely inhibit senescence but has the ability to antagonize CSE-induced cellular senescence in HBECs. |
| Regulatory pathway: | IGF-AKT-MTOR |
| R-AG-Pathway: | Downregulation |
| Official symbol(s): | IGF1-AKT1-MTOR |
| Pathway experiment: | Knockdown//Western blot |
| Pathway description: | SIRT6 knockdown and mutant SIRT6 H133Y overexpression enhanced phosphorylation of IGF-1R accompanied by a modest increase in IGF-1R expression. Next, we examined phosphorylation of Akt and S6K. Consistent with IGF-1R phosphorylation, overexpression of SIRT6 clearly diminished Akt and S6K phosphorylation regardless of presence or absence of CSE. In contrast, SIRT6 knockdown and mutant SIRT6 H133Y overexpression induced Akt and S6K phosphorylation . |
Annotation:
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