For research use only
| Cat No. | ABC-X0345C |
| Product Type | Overexpression Stable Cell Lines |
| Cell Type | Fibroblast |
| Species | Human |
| Host Cell | NIH/3T3 |
| Source Organ | Embryo |
| Disease | Normal |
| Storage | Liquid Nitrogen |
Human FGFR3 (S249C_V555M) NIH/3T3 Cell Line, FGFR3, NIH/3T3, Overexpression Stable Cell Lines, Transfected Stable Cell Lines
Human FGFR3 (S249C_V555M) NIH/3T3 Overexpression Cell Line is a genetically engineered model derived from selected murine NIH/3T3 fibroblast parental cells based on customers’ requirement. FGFR3 (S249C_V555M) NIH/3T3 overexpression cell line is generated by stable integration of exogenous human FGFR3 double mutant (S249C and V555M) into NIH/3T3 host cells using our optimized transduction of lentiviral vectors. The expression cassette contains the full-length FGFR3 open reading frame carrying both activating mutations. The edited cells are maintained at low passage numbers (<P20). Overexpression clone is validated at gene level by qRT-PCR. Target FGFR3 (Fibroblast Growth Factor Receptor 3) is a receptor tyrosine kinase involved in cell growth, differentiation, and angiogenesis. Mutations like S249C and V555M are recurrent in cancers such as bladder cancer and multiple myeloma, and lead to ligand-independent activation and downstream oncogenic signaling. 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-X0345C |
| Product Category | Transfected Stable Cell Lines |
| Size/Quantity | 1 vial |
| Cell Type | Fibroblast |
| Growth Mode | Adherent |
| Shipping Info | Dry Ice |
| Growth Conditions | 37 °C, 5% CO2 |
| Source Organ | Embryo |
| Disease | Normal |
| Biosafety Level | 1 |
| Storage | Liquid Nitrogen |
| Product Type | Overexpression Stable Cell Lines |
| Host Cell | NIH/3T3 |
| Quality Control | All cells test negative for mycoplasma, bacteria, yeast, and fungi. |
This cell line is designed to support studies of FGFR3-driven oncogenic transformation, particularly the S249C and V555M double mutation frequently observed in bladder cancer and skeletal dysplasias. It enables in vitro screening of FGFR inhibitors, elucidation of downstream signaling events, and investigation of tumorigenic pathways involving MAPK and PI3K-AKT cascades. It is suitable for drug sensitivity profiling and mechanistic studies in fibroblast-based systems that mimic cancer-associated genetic alterations.