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-SC016370
Host Cell : HEK293 (CHO and other cell types are also available) Size : >1x106 frozen cells/vial
| Cat. No. | CSC-SC016370 |
| 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 | TNFRSF9 |
| 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 | TNFRSF9 tumor necrosis factor receptor superfamily, member 9 [ Homo sapiens ] |
| Gene Symbol | TNFRSF9 |
| Synonyms | TNFRSF9; tumor necrosis factor receptor superfamily, member 9; ILA; tumor necrosis factor receptor superfamily member 9; 4 1BB; CD137; CD137 antigen; T cell antigen ILA; T-cell antigen ILA; 4-1BB ligand receptor; homolog of mouse 4-1BB; receptor protein 4-1BB; T-cell antigen 4-1BB homolog; induced by lymphocyte activation (ILA); interleukin-activated receptor, homolog of mouse Ly63; 4-1BB; CDw137; MGC2172; FLJ43501; |
| GeneID | 3604 |
| Uni ProtID | Q07011 |
| mRNA Refseq | BC006196 |
| Chromosome Location | 1p36 |
| Function | binding; receptor activity; |
| Pathway | Cytokine-cytokine receptor interaction, organism-specific biosystem; Cytokine-cytokine receptor interaction, conserved biosystem; Downstream signaling in naive CD8+ T cells, organism-specific biosystem; |
| MIM | 602250 |
Breast cancer is the most common cancer in women worldwide. Endocrine therapy is effective in 85% of breast cancer patients, but 15% are left with chemotherapy and surgery, which carries a poor prognosis. Immunotherapy is a novel treatment option for breast cancer, with PD-1 and CTLA-4 antibodies demonstrating immunomodulatory effects in breast cancer drug trials. Here, researchers discovered that TNFRSF9 regulates breast cancer cell proliferation, invasion, and apoptosis by regulating p38 phosphorylation, which in turn regulates PAX6 expression. TNFRSF9 levels were significantly reduced in breast cancer tissues and cell lines, and knockdown of TNFRSF9 promoted breast cancer cell development and progression. Furthermore, researchers found that downregulating TNFRSF9 upregulated phosphorylated p38 (p-p38) and PAX6 expression. A p38 phosphorylation inhibitor reversed PAX6 upregulation, inhibiting breast cancer cell proliferation and invasion and promoting apoptosis. This study proposes a novel TNFRSF9/p38/PAX6 axis that contributes to tumor suppression, suggesting a potential immunotherapy target for breast cancer.
Here, researchers investigated the role of TNFRSF9 gene deregulation in tumor development. Transwell assays were used to assess cell invasion (Figures 1a and b). Compared with the negative control, the TNFRSF9 knockdown in both MCF-7 and ZR-75-30 cell lines enhanced cell invasion, whereas the TNFRSF9 overexpression in both MCF-7 and ZR-75-30 cell lines inhibited cell invasion. Flow cytometry was used to assess apoptosis in both cell lines (Figures 1c and d). In the TNFRSF9 overexpressing cell lines, the apoptosis rate was reduced. These results suggest that TNFRSF9 is a suppressor of breast cancer malignancy and that activation of TNFRSF9 can inhibit breast cancer progression.
Figure 1 (a, b). Transwell assays were used to assess
cell invasion. (Liu X, et al., 2022)
Figure 1 (c-d). The cell apoptosis was examined through flow cytometry in both cell
lines. (Liu X, et al., 2022)
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