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Panoply™ Human TBK1 Over-expressing Stable Cell Line

For research use only. Not intended for any clinical use.

Cat. No. :   CSC-SC015668

Host Cell :   HEK293 (CHO and other cell types are also available) Size :   >1x106 frozen cells/vial

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Cell Line Information

Cell Culture Information

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Gene Information

Cat. No. CSC-SC015668
Description Using Creative Biogene's proprietary lentiviral vectors, we subclone the target gene into lentivector, generate the lentivirus particles, sequentially infect the cell line HEK293 (other cell types are also available according to your requirements), and select the clones constantly expressing target gene at high level.
Target Gene TBK1
Gene Species Homo sapiens (Human)
Host Cell HEK293 (CHO and other cell types are also available)
Host Cell Species Species varies
Applications

1. Gene expression studies

2. Signaling pathway research

3. Drug screening and toxicology

4. Disease research

Size 2 × 10^6 cells / vial
Stability Validated for at least 10 passages
Quality Control Negative for bacteria, yeast, fungi and mycoplasma.
Storage Liquid nitrogen
Shipping Dry Ice
Revival Rapidly thaw cells in a 37°C water bath. Transfer contents into a tube containing pre-warmed media. Centrifuge cells and seed into a 25 cm2 flask containing pre-warmed media.
Mycoplasma Negative
Format One frozen vial containing millions of cells
Storage Liquid nitrogen
Safety Considerations The following safety precautions should be observed.
1. Use pipette aids to prevent ingestion and keep aerosols down to a minimum.
2. No eating, drinking or smoking while handling the stable line.
3. Wash hands after handling the stable line and before leaving the lab.
4. Decontaminate work surface with disinfectant or 70% ethanol before and after working with stable cells.
5. All waste should be considered hazardous.
6. Dispose of all liquid waste after each experiment and treat with bleach.
Ship Dry ice
Gene Name TBK1 TANK-binding kinase 1 [ Homo sapiens ]
Gene Symbol TBK1
Synonyms TBK1; TANK-binding kinase 1; serine/threonine-protein kinase TBK1; NAK; NF-kB-activating kinase; NF-kappa-B-activating kinase; T2K; FLJ11330;
GeneID 29110
Uni ProtID Q9UHD2
mRNA Refseq BC034950
Chromosome Location 12q14.2
Function ATP binding; nucleic acid binding; nucleotide binding; phosphoprotein binding; protein binding; protein kinase activity; protein serine/threonine kinase activity;
Pathway Activated TLR4 signalling, organism-specific biosystem; Activation of IRF3/IRF7 mediated by TBK1/IKK epsilon, organism-specific biosystem; Cytosolic DNA-sensing pathway, organism-specific biosystem; Cytosolic DNA-sensing pathway, conserved biosystem; Cytosolic sensors of pathogen-associated DNA, organism-specific biosystem; DAI mediated induction of type I IFNs, organism-specific biosystem; Hepatitis C, organism-specific biosystem;
MIM 604834
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Thyroid cancer is receiving increasing attention. However, its detailed pathogenesis and pathological processes remain unclear. Here, researchers investigated the role of TANK-binding kinase 1 (TBK1) in the progression of thyroid cancer. The study showed that TBK1 is highly expressed in thyroid tumors. High expression of TBK1 enhances the viability, proliferation, migration, and invasion of thyroid cancer cells. Gene set enrichment analysis revealed that TBK1 activates the phosphatidylinositol-3-kinase/protein kinase B/target of rapamycin (PI3K/PKB/mTOR) signaling pathway. Furthermore, Myc-associated zinc finger protein (MAZ) is overexpressed in thyroid cancer and transcribes and activates TBK1. MAZ silencing reversed the effect of TBK1 overexpression on thyroid cancer progression. Co-transfection of MAZ small interfering RNA (siRNA) with TBK1 siRNA did not enhance the inhibitory effect of TBK1 silencing on thyroid cancer cells. Xenograft experiments showed that TBK1 short hairpin RNA inhibited tumor growth. Therefore, MAZ silencing inhibits tumor progression of thyroid cancer cells, while TBK1 overexpression reverses this inhibitory effect.

To investigate the role of TBK1 in thyroid cancer, researchers conducted TBK1 overexpression and knockdown experiments. The results showed that both overexpression plasmids and siRNA effectively regulated TBK1 expression (Figure 1A-C). High TBK1 expression significantly enhanced the viability of thyroid cancer cells (Figure 1D). Proliferation of TBK1-overexpressing cells was promoted, while proliferation of TBK1-silenced cells was inhibited (Figure 1E, F). TBK1 overexpression significantly increased the wound healing rate of TPC-1 and CAL-62 cells, while TBK1 silencing reduced the wound healing rate of thyroid cancer cells (Figure 1G, H). As shown in Figure 1I,J, the invasion cell number in TBK1-verexpressed thyroid cancer cells was markedly raised, whereas TBK1 silencing suppressed the invasion.

Figure 1. TBK1 promotes the proliferation of thyroid cancer cells.Figure 1. TBK1 promotes the proliferation of thyroid cancer cells. (Jiang Q, et al., 2023)

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