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-DC008319
Host Cell : HEK293 (Hela and other cell types are also available) Validation : Real-Time RCR
| Cat. No. | CSC-DC008319 |
| 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 | KLRB1 |
| 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 | KLRB1 killer cell lectin-like receptor subfamily B, member 1 [ Homo sapiens ] |
| Gene Symbol | KLRB1 |
| Synonyms | NKR; CD161; CLEC5B; NKR-P1; NKRP1A; NKR-P1A; hNKR-P1A |
| Gene Description | killer cell lectin-like receptor subfamily B, member 1 |
| GeneID | 3820 |
| Uni ProtID | Q12918 |
| mRNA Refseq | NM_002258.2 |
| Protein Refseq | NP_002249.1 |
| Chromosome Location | 12p13 |
| Function | carbohydrate binding; transmembrane signaling receptor activity; |
| Pathway | Malaria, organism-specific biosystem; Malaria, conserved biosystem; |
| MIM | 602890 |
Lung cancer is the most common primary malignant tumor of the lung. As one of the malignant tumors that poses the greatest threat to human health, its incidence has remained high in recent years. Previous studies have shown that KLRB1 is transcriptionally repressed in lung adenocarcinoma and is associated with the prognosis of lung adenocarcinoma. Here, the researchers explored the intrinsic mechanism by which KLRB1 affects the malignant phenotypes of lung adenocarcinoma, such as immune infiltration, proliferation, growth, and metastasis. Studies have shown that KLRB1 expression in lung cancer tissue is lower than that in surrounding healthy tissue. In the KLRB1 low expression group and high expression group, differentially expressed genes were significantly enriched in immune-related pathways. KLRB1 regulates the growth and proliferation of lung adenocarcinoma cells by affecting the MAPK/ERK signaling pathway. KLRB1 expression is associated with the prognosis, immune infiltration, cell migration and proliferation of lung adenocarcinoma (LUAD).
Here, researchers constructed KLRB1 knockdown A549 cells to examine the role of KLRB1 in lung cancer cells. RT-qPCR and Western blot analysis demonstrated that siRNA suppressed KLRB1 expression in A549 cells (Figures 1A and 1B). The researchers assessed the migration and invasion abilities of control (NC) and KLRB1 knockdown A549 cells. Results showed that KLRB1 knockdown cells significantly enhanced their migration and invasion abilities compared with control cells (Figure 1C). These results suggest that KLRB1 depletion increases the metastatic potential of lung cancer cells in vitro. A CF assay was performed to assess the clonogenicity of KLRB1. Results demonstrated that reduced KLRB1 levels significantly enhanced the CF ability of A549 cells (Figure 1D). CCK-8 analysis demonstrated that KLRB1 knockdown significantly increased A549 cell viability (Figure 1E).
Figure 1. Silencing KLRB1 promoted the migration, invasion and proliferation of lung adenocarcinoma cells in vitro. (Xu S, et al., 2024)
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