For research use only
| Cat No. | ABC-X0362C |
| Product Type | Overexpression Stable Cell Lines |
| Cell Type | Glioblastoma Cell |
| Species | Human |
| Host Cell | LN18 |
| Source Organ | Brain |
| Disease | Glioblastoma |
| Storage | Liquid Nitrogen |
LN18 cells stably expressing human MTAP, useful in methylation metabolism, glioblastoma studies, and evaluating therapeutic vulnerability in MTAP deletions.
MTAP LN18 Overexpression Cell Line is a genetically engineered model derived from selected human glioblastoma (LN18) parental cell line based on customers’ requirement. MTAP LN18 overexpression cell line is generated by stable integration of exogenous human MTAP into LN18 host cells using our optimized transduction of lentiviral vectors. Overexpression clone is validated at gene level by qRT-PCR.
Target
The MTAP gene encodes methylthioadenosine phosphorylase, an enzyme involved in the methionine salvage pathway and purine metabolism. MTAP deletion is frequently observed in cancers such as glioblastoma, pancreatic cancer, and mesothelioma, contributing to tumorigenesis and metabolic vulnerabilities. Its overexpression allows investigation of tumor suppression and synthetic lethality pathways. 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-X0362C |
| Product Category | Transfected Stable Cell Lines |
| Size/Quantity | 1 vial |
| Cell Type | Glioblastoma Cell |
| Growth Mode | Adherent |
| Shipping Info | Dry Ice |
| Growth Conditions | 37 °C, 5% CO2 |
| Source Organ | Brain |
| Disease | Glioblastoma |
| Biosafety Level | 1 |
| Storage | Liquid Nitrogen |
| Product Type | Overexpression Stable Cell Lines |
| Host Cell | LN18 |
| Quality Control | All cells test negative for mycoplasma, bacteria, yeast, and fungi. |
The MTAP LN18 Overexpression Cell Line serves as a powerful tool to investigate MTAP-related metabolic regulation and drug sensitivity. This model enables mechanistic studies of purine metabolism, methylation, and targeted synthetic lethality in MTAP-deficient tumors. It is utilized for screening MTAP-replacement strategies and MTAP-co-deletion associated vulnerabilities.