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-DC005722
Host Cell : HEK293 (Hela and other cell types are also available) Validation : Real-Time RCR
| Cat. No. | CSC-DC005722 |
| 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 | FGFR3 |
| 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 | FGFR3 fibroblast growth factor receptor 3 [ Homo sapiens ] |
| Gene Symbol | FGFR3 |
| Synonyms | ACH; CEK2; JTK4; CD333; HSFGFR3EX |
| Gene Description | fibroblast growth factor receptor 3 (achondroplasia, thanatophoric dwarfism) |
| GeneID | 2261 |
| Uni ProtID | P22607 |
| mRNA Refseq | NM_001163213.1 |
| Protein Refseq | NP_001156685.1 |
| Chromosome Location | 4p16.3 |
| Function | ATP binding; fibroblast growth factor binding; fibroblast growth factor binding; fibroblast growth factor-activated receptor activity; protein binding; protein tyrosine kinase activity; |
| Pathway | Adaptive Immune System, organism-specific biosystem; Bladder cancer, organism-specific biosystem; Bladder cancer, conserved biosystem; Constitutive PI3K/AKT Signaling in Cancer, organism-specific biosystem; DAP12 interactions, organism-specific biosystem; DAP12 signaling, organism-specific biosystem; Disease, organism-specific biosystem; |
| MIM | 134934 |
Dysregulation of the FGF/FGFR signaling pathway within the fibroblast growth factor receptor (FGFR) family is closely associated with tumorigenesis, progression, and resistance to anticancer drugs. Fibroblast growth factor receptor 3 (FGFR3) is a member of this family. Here, researchers investigated the effects of FGFR3 knockdown on the biological behavior of intrahepatic cholangiocarcinoma (ICC) cells. Their study found that FGFR3 knockdown inhibited ICC cell migration, invasion, and proliferation through scratch assays, Transwell migration and invasion assays, and cell proliferation assays. FGFR3 knockdown significantly downregulated the protein expression levels of MMP2, cyclin D1, and N-cadherin, but had no significant effect on the protein expression levels of MMP9, cyclin D3, vimentin, and E-cadherin. Furthermore, bioinformatics analysis and Western blotting experiments confirmed that ERK/c-Myc may be its signaling pathway. In conclusion, FGFR3 knockdown inhibits the migration, invasion, and proliferation of ICC cells. This suggests that FGFR3 may be a therapeutic target for ICC and could potentially improve the cure rate for patients with intrahepatic cholangiocarcinoma who receive FGFR inhibitor therapy.
To investigate whether FGFR3 expression affects the migration and invasion abilities of RBE cells, researchers conducted scratch wound healing, Transwell migration, and Transwell invasion assays. The scratch wound healing assay showed that FGFR3-knockdown RBE cells had significantly lower migration ability than the negative control group (Figures 1A and 1B). The Transwell migration assay showed similar results (Figures 1C and 1D). Furthermore, the Transwell invasion assay showed that FGFR3-knockdown RBE cells had significantly lower invasive ability than control cells (Figures 1C and 1E). Subsequently, researchers analyzed MMP expression levels using Western blotting. The results showed that, compared to the control group, MMP2 expression was significantly downregulated in FGFR3-knockdown cells, while MMP9 expression remained largely unchanged.
Figure 1. Knockdown expression of FGFR3 suppressed ICC cell migration and invasion. (Chen Y, et al., 2023)
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