For research use only
| Cat No. | ABC-X0059C |
| Product Type | Overexpression Stable Cell Lines |
| Cell Type | Lymphocytes |
| Species | Human |
| Host Cell | BAF3 |
| Source Organ | Lymphatic |
| Disease | Normal |
| Storage | Liquid Nitrogen |
This engineered BAF3 cell line expressing KIF5B-RET (I788N) fusion enables functional study of RET mutations and testing of RET-targeted agents.
The Human KIF5B_RET (I788N) BAF3 Cell Line is a genetically engineered model derived from the murine pro-B cell line BAF3 based on customers’ requirement. This overexpression cell line is generated by stable integration of exogenous human KIF5B_RET (I788N) fusion gene into BAF3 host cells using our optimized transduction of lentiviral vectors. Overexpression clone is validated at gene level by qRT-PCR.
Target
The KIF5B_RET (I788N) fusion combines the motor protein KIF5B with the receptor tyrosine kinase RET, harboring the I788N mutation. This genetic alteration confers constitutive kinase activation, leading to aberrant cell growth and survival through MAPK and PI3K/AKT pathways. RET fusion events are recurrent in lung adenocarcinomas and thyroid cancers. 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-X0059C |
| 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. |
The Human KIF5B_RET (I788N) BAF3 Cell Line provides a relevant model for dissecting RET fusion-driven oncogenesis and for evaluating selective RET inhibitors. This system supports drug screening, resistance mechanism analysis, and RET-targeted therapeutic development in solid tumor contexts.