Description
This assay uses the Luminex® 200™ platform.
Introducing our most comprehensive mouse array, featuring two assays conducted simultaneously from a single small sample volume: MD32 and MD12. By running both assays concurrently, we ensure efficient and high-quality results, providing you with the insights from two distinct assays in a swift turnaround time. This streamlined approach optimizes your workflow and accelerates your research outcomes.
Consider this assay for a detailed analysis of cytokines and chemokines in mouse models. The Mouse Cytokine/Chemokine 44-Plex Discovery Assay® Array (MD44) measures 44 biomarkers, including IL-6, TNFα, and VEGF-A, offering a comprehensive view of immune and inflammatory responses.
This panel is particularly useful for studying complex conditions such as cancer, autoimmune diseases, and chronic infections. For example, VEGF-A is significant in tumor angiogenesis, while IL-6 and TNFα are involved in inflammatory pathways seen in diseases like rheumatoid arthritis and lupus. The assay also helps in examining immune responses to infections with biomarkers like IFNγ and MCP-1.
Discover the power of precision with our assay, expertly designed for the Luminex® 200™ platform. This cutting-edge technology enables the simultaneous detection of multiple biomarkers from a minimal single sample, delivering comprehensive insights with unmatched efficiency. Streamline your research and unlock a new level of detail with our advanced multiplex assay solution.
Recommended Dilution: The kit manufacturer recommends Serum and Plasma be run at a 2-fold dilution. If you wish to run your samples at a dilution, predilute your samples with PBS pH~7.5. See our Sample Dilution Guide for more information.
If you expect your samples to have low cytokine levels, i.e. normal healthy populations, you may wish to inquire about a High Sensitivity panel.
Click here for information on shipping biological samples for Discovery Assays
Published Research Featuring Our MD44:
- PNAS! Tuffs, S. W., Goncheva, M. I., Xu, S. X., & McCormick, J. K. (2022). Superantigens promote Staphylococcus aureus bloodstream infection by eliciting pathogenic interferon-gamma production. Microbiology.
- Maus, M., López-Polo, V., Mateo, L., Lafarga, M., Aguilera, M., De Lama, E., Meyer, K., Sola, A., Lopez-Martinez, C., López-Alonso, I., Guasch-Piqueras, M., Hernandez-Gonzalez, F., Chaib, S., Rovira, M., Sanchez, M., Faner, R., Agusti, A., Diéguez-Hurtado, R., Ortega, S., Manonelles, A., Engelhardt, S., Monteiro, F., Stephan-Otto Attolini, C., & Prats, N. (2023). Iron accumulation drives fibrosis, senescence, and the senescence-associated secretory phenotype. Nature Metabolism, 5, 2111–2130.
- Wang, Z., Goto, Y., Allevato, M. M., Wu, V. H., Saddawi-Konefka, R., Gilardi, M., Alvarado, D., Yung, B. S., O’Farrell, A., Molinolo, A. A., Duvvuri, U., Grandis, J. R., Califano, J. A., Cohen, E. E. W., & Gutkind, J. S. (2021). Disruption of the HER3-PI3K-mTOR oncogenic signaling axis and PD-1 blockade as a multimodal precision immunotherapy in head and neck cancer. Nature Communications, 12, Article 2383.
- Redgrave, R. E., Dookun, E., Booth, L. K., Camacho Encina, M., Folaranmi, O., Tual-Chalot, S., Gill, J. H., Owens, W. A., Spyridopoulos, I., Passos, J. F., & Richardson, G. D. (2023). Senescent cardiomyocytes contribute to cardiac dysfunction following myocardial infarction. npj Aging, 9, Article 15.