Transfected Stable Cell Lines
Reliable | High-Performance | Wide Rage
Precision reporter, kinase, immune receptor, biosimilar, Cas9, and knockout stable cell lines for diverse applications.
Cat. No. : CSC-DC015668
Host Cell : HEK293 (Hela and other cell types are also available) Validation : Real-Time RCR
| Cat. No. | CSC-DC015668 |
| Description | Creative Biogene's Knockdown Cell Lines are target specific shRNA lentivirus transduced cells. The percent knockdown levels range from 75-99% depending on the gene, as evaluated by Real-Time RCR. Cells are rigorously qualified and mycoplasma free. |
| Target Gene | TBK1 |
| Host Cell | HEK293 (Hela and other cell types are also available) |
| Host Cell Species | Homo sapiens (Human) |
| Applications |
(1) Studying gene functions (2) Studying gene interactions and signaling pathways (3) Target validation and drug discovery (4) Designing diseases models |
| Size | >1 × 106 cells / vial |
| Stability | Validated for at least 10 passages |
| Validation | Real-Time RCR |
| Quality Control | Negative for bacteria, yeast, fungi and mycoplasma. |
| Storage | Liquid Nitrogen |
| Shipping | Dry Ice |
| 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 |
Cholangiocarcinoma (CCA) is a highly heterogeneous and metastatic malignant tumor with a poor prognosis even after radical hepatectomy. Here, researchers found that serine/threonine protein kinase TANK-binding kinase 1 (TBK1) exhibits dynamic changes at different stages of spontaneous CCA carcinogenesis in mice (hyperplasia, dysplasia, and CCA). Compared to non-tumor tissues, TBK1 is highly expressed in human tissues, including intrahepatic (n=182) and extrahepatic (n=40) CCA tissues, and elevated TBK1 expression is positively correlated with tumor diameter increase, lymph node metastasis, and TNM stage progression. Functional studies showed that TBK1 promotes CCA growth and metastasis both in vitro and in vivo. TBK1 directly interacts with β-catenin, promoting its phosphorylation at the S552 site and its nuclear translocation, thereby activating EMT-related transcriptional reprogramming. The TBK1 inhibitor GSK-8612 or a kinase-inactivating mutant effectively inhibited this process.
To elucidate the role of TBK1 in the progression of cholangiocarcinoma (CCA), researchers knocked down TBK1 expression in HuCCT1 cells, which have relatively high levels of endogenous TBK1. Furthermore, they overexpressed TBK1 in TFK1 cells, which have relatively low levels of endogenous TBK1. CCK8 assays showed that cell proliferation was inhibited in TBK1-knockdown cells. Scratch-migration, Transwell migration, and Matrigel invasion assays demonstrated that the growth, migration, and invasion abilities of TBK1-knockdown cells were weakened (Figures 1A and 1B). Conversely, TBK1 overexpression significantly enhanced these effects.
Figure 1. TBK1 promotes CCA cell growth, migration, and invasion. (Gao C Q, et al., 2023)
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