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-SC011962
Host Cell : HEK293 (CHO and other cell types are also available) Size : >1x106 frozen cells/vial
| Cat. No. | CSC-SC011962 |
| 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 | PLK1 |
| 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 | PLK1 polo-like kinase 1 [ Homo sapiens ] |
| Gene Symbol | PLK1 |
| Synonyms | PLK; STPK13 |
| Gene Description | polo-like kinase 1 (Drosophila) |
| Gene ID | 5347 |
| Uni Prot ID | P53350 |
| m RNA Refseq | NM_005030.3 |
| Protein Refseq | NP_005021.2 |
| Chromosome Location | 16p12.2 |
| Function | ATP binding; anaphase-promoting complex binding; microtubule binding; protein binding; protein kinase activity; protein kinase binding; protein serine/threonine kinase activity; protein serine/threonine kinase activity; |
| Pathway | APC/C-mediated degradation of cell cycle proteins, organism-specific biosystem; APC/C:Cdh1 mediated degradation of Cdc20 and other APC/C:Cdh1 targeted proteins in late mitosis/early G1, organism-specific biosystem; Activation of APC/C and APC/C:Cdc20 mediated degradation of mitotic proteins, organism-specific biosystem; Cell Cycle, organism-specific biosystem; Cell Cycle, Mitotic, organism-specific biosystem; Cell cycle, organism-specific biosystem; Cell cycle, organism-specific biosystem; |
| MIM | 602098 |
Minichromosome maintenance 3 (MCM3) protein has been extensively studied due to its crucial role in DNA replication. Furthermore, it is overexpressed in various human tumors. However, the role of this protein in renal cell carcinoma (RCC) remains largely unknown. Here, researchers demonstrate that Polo-like kinase 1 (PLK1)-mediated MCM3 phosphorylation regulates the proliferation and apoptosis of RCC cells. PLK1 and phospho-MCM3 (p-MCM3) are highly expressed in renal cell carcinoma. PLK1 expression is closely associated with the clinical characteristics of renal cell carcinoma. They play important roles in RCC proliferation and apoptosis. In vitro experiments showed that overexpression of PLK1 or MCM3 significantly enhanced RCC cell proliferation and inhibited apoptosis; conversely, knockdown of PLK1 or MCM3 reduced RCC cell proliferation and increased apoptosis. Moreover, MCM3 is a physiological substrate of PLK1 and is phosphorylated at serine 112 (Ser112) in a PLK1-dependent manner. PLK1-mediated MCM3 phosphorylation promotes RCC cell cycle progression and inhibits apoptosis in vitro. In summary, PLK1-mediated MCM3 phosphorylation is a novel mechanism regulating RCC proliferation and apoptosis.
The malignant progression and poor prognosis of renal cell carcinoma (RCC) are associated with elevated PLK1 expression. To investigate whether PLK1 plays a key role in the viability and proliferation of RCC cells, researchers performed MTT and colony formation assays. Compared to control cells, PLK1-overexpressing 786-O and ACHN cells showed significantly increased cell viability and proliferation. Conversely, inhibiting PLK1 expression significantly suppressed the viability and proliferation of 786-O and ACHN cells (Figure 1a-d). 5-ethynyl-2'-deoxyuridine (EdU) incorporation experiments also showed similar results (Figure 1e, f). These results indicate that PLK1 enhances the viability and proliferative capacity of RCC cells.
Figure 1. PLK1 promotes cell viability and proliferation of RCC cells in vitro. (Gao Z, et al., 2020)
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