External factors
| External factors: |
TBK1-II |
| Category: |
Chemical compounds |
| Experimental category: |
HL |
| Tissue type: |
Mammary Gland |
| Cell name: |
HCC1954,SK-BR-3,Neu monolayer cell |
| 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. |
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Regulatory relationship
| 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. |
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Aging network
Annotation:
The green line represents Upregulation.
The purple line represents Downregulation.
The orange line represents Activation.
The yellow line represents Inhibition.
The gray line represents Unclear.
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