Cat.No. : CSC-SC001446 Host Cell: HEK293 (CHO and other cell types are also available)
| Cat. No. | CSC-SC001446 |
| 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. |
| Gene | BIRC5 |
| Gene Species | Homo sapiens (Human) |
| Host Cell | HEK293 (CHO and other cell types are also available) |
| Stability | Validated for at least 10 passages |
| Application | 1. Gene expression studies 2. Signaling pathway research 3. Drug screening and toxicology 4. Disease research |
| Quality Control | Negative for bacteria, yeast, fungi and mycoplasma. |
| Size Form | 2 × 10^6 cells / vial |
| Shipping | Dry Ice |
| Storage | Liquid nitrogen |
| 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. |
| 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 |
| UniProt ID | H3BLT4 |
| mRNA 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 |
| 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 |
Colorectal cancer (CRC) is one of the most common human malignancies. Alterations in the DNA damage response (DDR) pathway are emerging as novel therapeutic targets for various cancer types, including CRC. RFWD3 plays a key role in replication protein A (RPA)-mediated DNA damage in cancer cells. Importantly, RFWD3 can respond to DNA damage by positively regulating p53 stability during G1 cell cycle checkpoint activation. Here, researchers show that knockdown of RFWD3 inhibits CRC development and progression in vitro and in vivo. Exploring the downstream mechanisms of RFWD3 action, researchers discovered that RFWD3 can transcriptionally activate BIRC5 through interaction with E2F transcription factor 1 (E2F1). Therefore, BIRC5 is a downstream gene of RFWD3 in CRC regulation. Subsequent loss- and gain-of-function experiments demonstrated that overexpression of BIRC5 in RFWD3-depleted RKO cells reversed the inhibitory effects on cell proliferation, migration, and colony formation, while also improving apoptosis, indicating that the effects of RFWD3 depletion are primarily due to BIRC5 inhibition.
To confirm the role of BIRC5 in RFWD3-mediated CRC, the researchers used BIRC5-overexpressing RKO cell, RFWD3-knockdown RKO cell, and RFWD3-knockdown combined with BIRC5-overexpressing RKO cell, and conducted in vitro experiments. Simultaneously, changes in cell phenotype in these RKO cell models were observed using Celigo-based methods, scratch healing/Transwell migration assays, and flow cytometry. Consistent with previous findings, RFWD3 silencing significantly inhibited cell proliferation and migration. Conversely, in BIRC5-overexpressing RKO cells, cell proliferation, migration, and colony formation were enhanced, while apoptosis was reduced. Importantly, overexpressing BIRC5 in RFWD3-knockdown RKO cells reversed the inhibitory effects on cell proliferation, migration, and colony formation, while apoptosis was also improved, indicating that the effects of RFWD3 depletion were primarily due to BIRC5 inhibition (Figures 1A-E).
Figure 1. Overexpression of BIRC5 alleviates the inhibitory effects of RFWD3 knockdown on colorectal cancer cells. (Xu F, et al., 2021)
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