| Gene name: | NAMPT |
| Aging type: | Prevent |
| Aging characteristic: |
| Tissue type: | -- |
| Cell name: | SMC |
| Gene ID: | 10135 |
| Category: | protein coding |
| Phenotype: | Atherosclerosis |
| Experimental category: | L |
| PMID: | 17307730 |
| Experiment: | SA-β-gal activity assay//Knockdown |
| Description: | In the longer lived HITC6 SMCs,lifespan extension by Nampt was even more striking, with an additional 6.3±0.3 population doublings or a 71 ±7% extension of lifespan.We quantified the proportion of senescent SMCs in successive subcultures incubated with 10 nM FK866, a concentration we determined reduced Nampt activity in SMCs to 22 ± 2% of baseline.Kaplan-Meier survival analysis revealed a substantially shortened senescence-free survival of Nampt-inhibited cells SMCs. In contrast, there was markedly extended senescence-free survival in Namptoverexpressing SMCs versus vector-infected cells. |
| Target gene: | SIRT1//P53 |
| Official symbol(s): | SIRT1//P53 |
| R-AG-Target gene: | Activation//Downregulation |
| Subcategory: | Unclear |
| Target gene experiment: | Western blot |
| Target gene description: | SMCs overexpressing Nampt had a 86 ± 4% (p=0.03, n =4) increase in SIRT1 activity. We were surprised to find that Nampt overexpression also modestly increased abundance of SIRT1 protein (1.3±0.3-fold, p =0.02), although not enough to fully account for the increased deacetylase activity.this agerelated increase in p53 was blunted in parallel cultures of SMCs overexpressing Nampt. Furthermore, the fraction of p53 that was acetylated on Lys-382 was substantially lower in Nampt-overexpressing SMCs than in control cells. This p53 modification was associated with a significantly increased rate of p53 degradation in Nampt-overexpressing SMCs, as assessed in SMCs incubated with cycloheximide. |
| Regulatory pathway: | -- |
| R-AG-Pathway: | -- |
| Pathway experiment: | -- |
| Pathway description: | -- |
Annotation:
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