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-DC001446
Host Cell : HEK293 (Hela and other cell types are also available) Validation : Real-Time RCR
| Cat. No. | CSC-DC001446 |
| 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 | BIRC5 |
| 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 | BIRC5 baculoviral IAP repeat containing 5 [ Homo sapiens ] |
| Gene Symbol | BIRC5 |
| Synonyms | API4; EPR-1 |
| Gene Description | baculoviral IAP repeat-containing 5 (survivin) |
| Gene ID | 332 |
| Uni Prot ID | H3BLT4 |
| m RNA Refseq | NM_001012271.1 |
| Protein Refseq | NP_001012271.1 |
| Chromosome Location | 17q25 |
| Function | Ran GTPase binding; chaperone binding; cobalt ion binding; cofactor binding; cysteine-type endopeptidase inhibitor activity; cysteine-type endopeptidase inhibitor activity involved in apoptotic process; enzyme binding; identical protein binding; metal ion binding; microtubule binding; microtubule binding; protein binding; protein heterodimerization activity; protein homodimerization activity; protein homodimerization activity; tubulin binding; zinc ion binding; zinc ion binding; |
| Pathway | Apoptosis, organism-specific biosystem; Apoptosis Modulation and Signaling, organism-specific biosystem; Aurora A signaling, organism-specific biosystem; Aurora B signaling, organism-specific biosystem; Cell Cycle, organism-specific biosystem; Cell Cycle, Mitotic, organism-specific biosystem; Colorectal cancer, organism-specific biosystem; |
| MIM | 603352 |
Lung adenocarcinoma (LUAD) is a prevalent type of thoracic cancer with a poor prognosis and high mortality rate. DNA methylation is a potential factor contributing to the development of LUAD, leading to chromosomal structural changes and potentially tumorigenesis. The baculoviral IAP repeat-encoded 5 (BIRC5) gene encodes the survivin protein, a multifunctional gene involved in tumor cell proliferation, migration, and invasion. Here, researchers identified eight hub genes with aberrant expression and significant alterations in DNA methylation in LUAD. BIRC5 is a marker significantly upregulated in tumor tissues. To investigate the role of BIRC5 in LUAD cell death, A549 cells and mouse xenografts were analyzed using flow cytometry, lactate dehydrogenase (LDH) release assays, and micro-PET imaging. The researchers found that BIRC5 expression was upregulated and associated with high mortality in LUAD patients. Mechanistically, knockdown of BIRC5 inhibited A549 cell proliferation and induced pyroptosis via the caspase3/GSDME signaling pathway. These findings suggest that BIRC5 may be a novel biomarker and therapeutic target for lung adenocarcinoma. Furthermore, the researchers discovered a new pathway by which inhibition of BIRC5 can induce pyroptosis in lung adenocarcinoma cells through the caspase3-GSDME pathway.
To further elucidate the in vivo function of BIRC5, the researchers generated a BIRC5 knockdown cell line (Figure 1a). The A549 cell line was then divided into three groups: control, si-BIRC5, and si-NC. The tumorigenicity of the cells from these different groups was assessed in xenografted mice. Static PET images were acquired 1 hour after 18F-FDG injection in the control, si-BIRC5, and si-NC groups. The researchers observed a significant reduction in tumor size in BIRC5 knockdown A549 xenografted mice compared to the NC group (Figure 1b). Furthermore, tumor volume and weight were significantly reduced in BIRC5 knockdown A549 xenografted mice compared to the NC group (Figures 1c-e). Cell viability and migration of A549 cells were assessed using CCK8 and Transwell assays. The results showed that BIRC5 inhibition significantly suppressed cell survival and migration (Figures 1f, g). These data demonstrate that BIRC5 silencing exhibits anti-cancer effects both in vivo and in vitro.
Figure 1. The BIRC5 deletion inhibits LUAD progression. (Zhang Q, et al., 2023)
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