For research use only
| Cat No. | ABC-X0038C |
| Product Type | Overexpression Stable Cell Lines |
| Cell Type | Epithelial |
| Species | Human |
| Host Cell | 293T |
| Source Organ | Kidney |
| Disease | Normal |
| Storage | Liquid Nitrogen |
The Xpress™ human DDR2 overexpression cell line (293T) provides a powerful tool for studying tumor progression and fibrosis, suitable for high-throughput.
Xpress™ Human DDR2 Over-expressing Cell Line (293T) is a genetically engineered model derived from HEK293T parental cells based on customers’ requirement. This overexpression cell line is developed by stable integration of exogenous human DDR2 gene into the 293T host cells using our optimized lentiviral transduction system.
Target
DDR2 (Discoidin Domain Receptor 2) is a receptor tyrosine kinase that binds to collagen and mediates extracellular matrix remodeling, cell adhesion, and epithelial-to-mesenchymal transition (EMT). Its overexpression and activation are implicated in tumor progression, fibrosis, and metastasis, particularly in squamous cell lung carcinoma and breast cancer. AcceGen offers stable overexpression models for a wide range of genes involved in cancer biology and regenerative medicine. Polyclonal or monoclonal is optional based on customers’ research needs.
| Species | Human |
| Cat.No | ABC-X0038C |
| Product Category | Transfected Stable Cell Lines |
| Size/Quantity | 1 vial |
| Cell Type | Epithelial |
| Growth Mode | Adherent |
| Shipping Info | Dry Ice |
| Growth Conditions | 37 °C, 5% CO₂ |
| Source Organ | Kidney |
| Disease | Normal |
| Biosafety Level | 1 |
| Storage | Liquid Nitrogen |
| Product Type | Overexpression Stable Cell Lines |
| Host Cell | 293T |
| Quality Control | All cells test negative for mycoplasma, bacteria, yeast, and fungi. |
The Xpress™ Human DDR2 Over-expressing Cell Line (293T) serves as a robust tool for studying DDR2-driven signaling cascades, drug response profiling, and fibrotic disease modeling. It is also suitable for high-throughput screening of DDR2-targeted therapeutics and mechanistic studies of tumor-stroma interactions.