Transfected Stable Cell Lines
Reliable | High-Performance | Wide Rage
Precision reporter, kinase, immune receptor, biosimilar, Cas9, and knockout stable cell lines for diverse applications.
Cat. No. : GK-0007
| Cat. No. | GK-0007 |
| Description | Leveraging two major technology platforms—KASP (Kompetitive Allele-Specific PCR) and TaqMan MGB probes—we provide cost-effective or ultra-high-specificity custom genotyping services for any species and any genetic locus. |
| Introduction | If the customer provides a specific genotyping RS number, we can perform custom development and offer SNP testing services upon receipt of mailed blood/tissue/cell samples. The customer needs to provide: 1. Sample materials such as cells (≥10^6 cells), tissue (≥300 mg), blood (≥1 ml), serum (≥1.5 ml), etc.; nucleic acid extraction is charged separately; 2. Genomic DNA (volume ≥30 μl, concentration ≥50 ng/μl), with purity OD260/280 between 1.7 and 1.9; 3. For the human genome, the RS number of the SNP locus must be provided. For other species without rs numbers, such as cattle, chickens, and fish, the exact 200 bp sequences flanking both upstream and downstream of the SNP locus must be provided, along with the mutation type at the SNP locus and whether any other linked loci exist within 25 bp upstream or downstream of the locus. We deliver: 1. SNP results (Excel spreadsheet); 2. Complete experimental report: amplification and reaction systems, primers involved, and probe sequences; Scatter plot of clustering results (KASP method) / Amplification curves and Ct value analysis (TaqMan MGB method). 3. Other relevant materials required by the customer. |
| Gene | TREM2 |
| Features | Genotyping Accuracy >99% |
| Applications | Research Use |
| Size | Box |
| Format | 100T |
| Note | All SNP kits are custom-developed and not available from stock. Primers and probes are individually designed and synthesized based on the RS numbers or target sequences provided by the customer. |
| Storage | -20℃ |
Mutations at the TREM2 gene locus are among the clinically most valuable rare variants in Alzheimer's disease genetic risk research. Since first reported in The New England Journal of Medicine in 2013, it has been validated by more than 60 independent studies worldwide; carriers have a 2- to 4-fold increased disease risk, and its risk effect strength ranks first among non-APOE gene variants. This locus is located in the ligand-binding domain of the TREM2 protein and promotes AD pathological progression through multiple mechanisms, including weakening microglial clearance of β-amyloid, impairing synaptic pruning function, and exacerbating neuroinflammatory responses; moreover, carriers show significantly altered soluble TREM2 levels in cerebrospinal fluid and plasma, which can serve as a dynamic monitoring marker of disease progression. With advances in the development of TREM2-targeted agonists and gene therapy strategies, TREM2 genotyping detection can be used not only for early risk stratification and intervention timing assessment in asymptomatic high-risk populations, but also to provide enrollment criteria for patients participating in targeted drug clinical trials, promoting a paradigm shift in Alzheimer's disease from "symptomatic treatment" to "risk prediction and precision intervention," with important clinical application prospects and public health value.
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