| External factors: | TBK1-II |
| Aging type: | Accelerate |
| Aging characteristic: |
| Category: | Chemical compounds |
| Phenotype: | Aging |
| Experimental category: | HL |
| Tissue type: | Mammary Gland |
| Cell name: | HCC1954,SK-BR-3,Neu monolayer cell |
| PMID: | 24487029 |
| Experiment: | SA-β-gal activity assay//Flow cytometry |
| Description: | Remarkably, large, β-galactosidase-positive cells were observed in ~20% of lenti-shRNATbk1 transduced, and TBK1-II treated cultures .Strikingly, TBK1-II treatment (2 μM) virtually eliminated accumulation of cells in all phases and dramatically increased the percentage of cells with >4N chromosomes (M3 gate). This effect was also observed by forward- and side-scattering flow cytometry analysis. |
| Target gene: | P16//P65-NFκB |
| R-EF-Target gene: | Activation//-- |
| Official symbol(s): | P16//P65-NFκB |
| Target gene experiment: | Western blot |
| Target gene description: | The NF-κB family proteins, RelA (p65), c-Rel, RelB, p50, and p52, bind to DNA as dimers, the most common being a p65-p50 heterodimer (43). P65-NFκB activity is induced by phosphorylation of serine536 (44). In untreated HER2+ BC cells, p65-NFκB was highly phosphorylated on serine536. Importantly, TBK1-II treatment of mouse and human HER2+ BC cells dramatically suppressed serine536-phosphorylation, hence activity of p65-NFκB. In addition, expression of the pro-senescence cyclin-dependent kinase inhibitor p16INK4A (45) was dramatically induced in both mouse and human HER2+ BC cells. |
| Regulatory pathway: | -- |
| R-EF-Pathway: | -- |
| Pathway experiment: | -- |
| Pathway description: | -- |
Annotation: