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-SC016355
Host Cell : HEK293 (CHO and other cell types are also available) Size : >1x106 frozen cells/vial
| Cat. No. | CSC-SC016355 |
| 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 | TNFRSF11B |
| 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 | TNFRSF11B tumor necrosis factor receptor superfamily, member 11b [ Homo sapiens ] |
| Gene Symbol | TNFRSF11B |
| Synonyms | OPG; TR1; OCIF |
| Gene Description | tumor necrosis factor receptor superfamily, member 11b (osteoprotegerin) |
| Gene ID | 4982 |
| Uni Prot ID | O00300 |
| m RNA Refseq | NM_002546.3 |
| Protein Refseq | NP_002537.3 |
| Chromosome Location | 8q24 |
| Function | cytokine activity; receptor activity; |
| Pathway | Apoptosis Modulation and Signaling, organism-specific biosystem; Cytokine-cytokine receptor interaction, organism-specific biosystem; Cytokine-cytokine receptor interaction, conserved biosystem; Monoamine Transport, organism-specific biosystem; Osteoblast Signaling, organism-specific biosystem; Osteoclast Signaling, organism-specific biosystem; Osteoclast differentiation, organism-specific biosystem; |
| MIM | 602643 |
TNFRSF11B is involved in the development and progression of various malignancies. However, its function in bladder cancer and its associated carcinogenic mechanisms are less well understood. Here, researchers evaluated the clinical significance of TNFRSF11B in bladder cancer and its associated signaling pathways through bioinformatics analysis. The expression levels of TNFRSF11B were measured in bladder tissue and bladder cancer cells. To investigate the effect of the PI3K/AKT pathway on TNFRSF11B, experiments were performed using the PI3K/AKT inhibitor LY294002. The results showed that TNFRSF11B was significantly upregulated in bladder cancer tissue and various bladder cancer cell lines. Inhibition of TNFRSF11B expression inhibited the proliferation, migration, and invasion of bladder cancer cells. Overexpression of TNFRSF11B, however, had the opposite effect. These findings were further confirmed by in vivo experiments. Furthermore, TNFRSF11B promotes the malignant progression of bladder cancer by regulating the PI3K/AKT pathway. In summary, TNFRSF11B is highly expressed in bladder cancer and plays an important role in promoting cancer through the PI3K/AKT pathway. Therefore, TNFRSF11B may become a potential prognostic marker for bladder cancer treatment.
To validate the mechanism by which TNFRSF11B promotes tumorigenesis through the PI3K/AKT pathway, researchers conducted rescue experiments to confirm its pro-proliferative effect on bladder cancer cells. TNFRSF11B-overexpressing cells were treated with the PI3K/AKT inhibitor LY294002. CCK-8 and LDH assays showed that LY294002 significantly reduced the cell viability of TNFRSF11B-overexpressing T24 and 5637 cells (Figure 1A and B). Transwell invasion and migration assays demonstrated that LY294002 significantly inhibited the invasion and migration of TNFRSF11B-overexpressing T24 and 5637 cells (Figure 1C and D). Wound healing assay further confirmed that LY294002 inhibited the migration of bladder cancer cells (Figure 1E). Furthermore, researchers investigated whether TNFRSF11B exerts its oncogenic effects by inhibiting apoptosis. Flow cytometry results showed that LY294002 reversed the inhibitory effect of TNFRSF11B overexpression on cell apoptosis. Therefore, TNFRSF11B promotes tumor progression by inhibiting apoptosis in bladder cancer cells.
Figure 1. LY294002 inhibits the cancer-promoting activity of TNFRSF11B via the PI3K/AKT pathway. (Deng H, et al., 2024)
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