For research use only
| Cat No. | ABC-X0005C |
| Product Type | Overexpression Stable Cell Lines |
| Cell Type | Lymphocyte |
| Species | Human |
| Host Cell | BAF3 |
| Source Organ | Lymphatic |
| Disease | Normal |
| Storage | Liquid Nitrogen |
The human ERBB2 (R678Q) BAF3 cell line provides a powerful tool for studying the tumor mechanisms of HER2 mutations, supporting IL-3 independent growth.
Human ERBB2 (R678Q) BAF3 Cell Line is a genetically engineered model derived from selected murine Ba/F3 parental cell line based on customers’ requirement. ERBB2 (R678Q) BAF3 mutant cell line is generated by stable integration of exogenous human ERBB2 gene harboring the R678Q point mutation into Ba/F3 host cells using our optimized transduction of lentiviral vectors.
Target
The ERBB2 (HER2) gene encodes a transmembrane receptor tyrosine kinase critical for cell signaling cascades that control proliferation and survival. The R678Q mutation lies in the juxtamembrane domain and has been associated with enhanced dimerization and receptor activation independent of ligand binding. This mutation contributes to oncogenesis by triggering sustained downstream signaling, notably through MAPK and PI3K/AKT pathways, and has been reported in lung adenocarcinoma and other solid tumors. AcceGen offers generation of stable mutation-specific or overexpression cell lines targeting any gene of your interest. Polyclonal or monoclonal is optional based on customers’ research needs.
| Species | Human |
| Cat.No | ABC-X0005C |
| 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 ERBB2 (R678Q) BAF3 Cell Line serves as a powerful tool to investigate HER2-juxtamembrane mutation-driven oncogenic mechanisms and therapeutic interventions. This model enables studies of dimerization-mediated activation, IL-3-independent growth, and resistance to tyrosine kinase inhibitors. It is utilized for high-throughput screening of HER2-targeted therapies and evaluation of combination treatment strategies.