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: