For research use only
| Cat No. | ABC-X0006C |
| Product Type | Overexpression Stable Cell Lines |
| Cell Type | Lymphocyte |
| Species | Human |
| Host Cell | BAF3 |
| Source Organ | Lymphatic |
| Disease | Normal |
| Storage | Liquid Nitrogen |
The FGFR3 (TACC3_Y373C) BAF3 cell line provides a powerful tool for investigating the mechanisms of tumors driven by FGFR3 fusion mutations.
Human FGFR3 (TACC3_Y373C) BAF3 Cell Line is a genetically engineered model derived from selected murine Ba/F3 parental cell line based on customers’ requirement. FGFR3 (TACC3_Y373C) BAF3 mutant cell line is generated by stable integration of exogenous human FGFR3 gene harboring the TACC3_Y373C composite mutation/fusion into Ba/F3 host cells using our optimized transduction of lentiviral vectors.
Target
The FGFR3-TACC3 fusion involves the fibroblast growth factor receptor 3 (FGFR3) and transforming acidic coiled-coil containing protein 3 (TACC3), often coupled with point mutations such as Y373C that enhance oncogenicity. The fusion promotes constitutive FGFR3 kinase activity, disrupted mitotic spindle regulation, and activation of MAPK/ERK and PI3K/AKT pathways. This composite alteration has been observed in glioblastoma, bladder cancer, and lung cancer, and represents a potential therapeutic target. AcceGen offers generation of stable overexpression or fusion gene cell lines targeting any gene or variant of your interest. Polyclonal or monoclonal is optional based on customers’ research needs.
| Species | Human |
| Cat.No | ABC-X0006C |
| Product Category | Transfected Stable Cell Lines |
| Size/Quantity | 1 vial |
| Cell Type | Lymphocyte |
| Growth Mode | Suspension |
| Shipping Info | Dry Ice |
| Growth Conditions | 37 °C, 5% CO₂ |
| Source Organ | Lymphatic |
| Disease | Normal |
| Biosafety Level | 1 |
| Storage | Liquid Nitrogen |
| Product Type | Overexpression Stable Cell Lines |
| Host Cell | BAF3 |
| Quality Control | All cells test negative for mycoplasma, bacteria, yeast, and fungi. |
The FGFR3 (TACC3_Y373C) BAF3 Cell Line serves as a powerful tool to investigate FGFR3 fusion- and mutation-driven oncogenic mechanisms and therapeutic interventions. This model enables studies of kinase activation, chromosomal instability, and drug response in hematopoietic systems. It is utilized for high-throughput screening of FGFR inhibitors and evaluation of synthetic lethality and combination therapies.