Cat.No. : CSC-RO0199 Host Cell: CHO-K1
| Cat. No. | CSC-RO0199 |
| Description | This cell line is engineered to stably overexpress the mouse Cd47 in CHO-K1 cells. |
| Introduction | This cell line is constructed by transfection of mouse CD47 antigen (Rh-related antigen, integrin-associated signal transducer) (Cd47) into CHO-K1, followed by stable cell selection. The expression of Cd47 has been analyzed through flow cytometry. |
| Gene | Cd47 |
| Gene Species | Mus musculus (Mouse) |
| Host Cell | CHO-K1 |
| Host Cell Species | Cricetulus griseus (Chinese hamster) |
| Stability | Validated for at least 10 passages |
| Application | 1. Studying the interactions between immune cells and cancer cells 2. Studying the mechanisms of resistance to immune checkpoint blockade 3. High-throughput screening 4. Drug target validation |
| Quality Control | Negative for bacteria, yeast, fungi and mycoplasma. |
| Shipping | Dry ice |
| Storage | Liquid nitrogen |
| Revival | Rapidly thaw cells in a 37°C water bath. Transfer contents into a tube containing pre-warmed media. Centrifuge cells and seed into a 25 cm2 flask containing pre-warmed media. |
| Mycoplasma | Negative |
| Format | One frozen vial containing millions of cells |
| Storage | Liquid nitrogen |
| Safety Considerations |
The following safety precautions should be observed. 1. Use pipette aids to prevent ingestion and keep aerosols down to a minimum. 2. No eating, drinking or smoking while handling the stable line. 3. Wash hands after handling the stable line and before leaving the lab. 4. Decontaminate work surface with disinfectant or 70% ethanol before and after working with stable cells. 5. All waste should be considered hazardous. 6. Dispose of all liquid waste after each experiment and treat with bleach. |
| Ship | Dry ice |
Tumor microenvironment (TME) targeting, especially with PD-1/PD-L1 inhibitors, is a promising cancer treatment strategy. Researchers investigated the role of CD47 in cancer immunotherapy. Targeting the tumor microenvironment (TME) with immune checkpoint blockade (ICB) agents like PD-1/PD-L1 inhibitors has shown promise. However, tumor-associated macrophages (TAMs) create an immunosuppressive TME, hindering ICB efficacy. Blocking the CD47/SIRPα pathway restores macrophage phagocytosis and enhances antitumor effects, especially in combination with PD-1/PD-L1 blockade. SMC18, a dual-targeting small molecule, disrupts CD47/SIRPα and PD-1/PD-L1 interactions, activating macrophages and T cells, inhibiting tumor growth, and improving therapeutic outcomes, suggesting its potential in cancer immunotherapy.
Figure 1. Utilizing microscale thermophoresis (MST), SMC18 was identified from a drug library by researchers. It binds SIRPα and PD-L1, disrupting CD47/SIRPα and PD-1/PD-L1 interactions, indicating its potential in modulating immune checkpoint pathways. (Jin S, et al., 2024)
Utilizing Creative Biogene's Mouse Cd47 Stable Cell Line - CHO-K1 can streamline the experimental procedure described above. This stable cell line provides a consistent expression of Cd47, allowing researchers to conduct relevant experiments directly without the need for Cd47 gene transfection or overexpression. Consequently, researchers can expedite drug screening and assessment processes, as well as evaluate the potential effects of compounds on the Cd47/SIRPα interaction, thereby saving time and resources. By employing this stable cell line, researchers can efficiently advance studies related to Cd47 and its associated pathways.
A: CHO cells were likely selected for their suitability for protein expression and glycosylation, facilitating studies on TIGIT biology, immune modulation, and therapeutic antibody development.
A: Stability and expression were likely assessed through methods such as flow cytometry, immunoblotting, or functional assays measuring TIGIT-mediated signaling or ligand binding, with continuous selection pressure applied.
A: Characterization may involve analysis of TIGIT glycosylation patterns, binding affinity to its ligands, downstream signaling pathways, and functional implications in T cell activation, exhaustion, or immune checkpoint blockade.
A: Quality control likely included confirmation of TIGIT expression levels, validation of its binding specificity and functional activity, assessment of off-target effects, and validation of phenotypic changes associated with TIGIT modulation.
A: Comparative analysis with primary immune cells or in vivo models helps validate the relevance of TIGIT expression in immune checkpoints, tumor immune evasion, and its potential as a target for cancer immunotherapy, guiding the development of TIGIT-targeted therapeutics.
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Exceptional stability! The Mouse Cd47 Stable Cell Line in CHO-K1 cells offers reliable and consistent expression of Cd47, ensuring robust results in my immunology research.
Simplifying complex studies! With stable Cd47 expression, I can delve deeper into immune evasion mechanisms with confidence, streamlining my experiments and accelerating discoveries.
Impressive performance! The Mouse Cd47 Stable Cell Line exceeds expectations, providing a solid foundation for investigating the role of Cd47 in cancer immunotherapy and autoimmune diseases.
Streamlining my workflow! Its stable expression simplifies data interpretation and enhances the efficiency of my assays, allowing for more precise and insightful analysis.
A valuable asset! This cell line has revolutionized my approach to studying immune checkpoint pathways, offering invaluable insights into Cd47-mediated immune regulation and potential therapeutic interventions.
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