For research use only
| Cat No. | ABC-X0347C |
| Product Type | Overexpression Stable Cell Lines |
| Cell Type | Lymphocytes |
| Species | Human |
| Host Cell | BAF3 |
| Source Organ | Lymphatic |
| Disease | Normal |
| Storage | Liquid Nitrogen |
Human FGFR3_TACC3 (R669G) BAF3 Cell Line, FGFR3, BAF3, Overexpression Stable Cell Lines, Transfected Stable Cell Lines
Human FGFR3_TACC3 (R669G) BAF3 Overexpression Cell Line is a genetically engineered model derived from murine BAF3 pro-B cells based on customers’ requirement. This cell line stably expresses the human FGFR3_TACC3 fusion gene containing the R669G mutation, introduced via lentiviral vector transduction. The edited cells are validated by qRT-PCR and maintained at low passage numbers (<P20). Target FGFR3-TACC3 is a fusion oncogene found in glioblastoma and bladder cancer, driving constitutive dimerization and aberrant activation of FGFR signaling. The R669G mutation enhances fusion-driven oncogenesis and confers resistance to some FGFR inhibitors. AcceGen offers generation of stable overexpression cell lines targeting any gene of your interest. Polyclonal or monoclonal is optional based on customers’ research needs.
| Species | Human |
| Cat.No | ABC-X0347C |
| Product Category | Transfected Stable Cell Lines |
| Size/Quantity | 1 vial |
| Cell Type | Lymphocytes |
| 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. |
This cell line overexpresses the FGFR3-TACC3 fusion with the R669G point mutation, representing a recurrent event in glioblastoma and other solid tumors. It supports studies on oncogenic fusion proteins, aberrant receptor tyrosine kinase signaling, and resistance to FGFR-targeted therapies. The model is highly useful for evaluating drug responses, understanding transformation potential, and modeling chromosomal rearrangement-driven tumorigenesis in hematopoietic cells.