The CD36 Knockout AGS Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed to disrupt the expression of the CD36 gene in the human AGS gastric epithelial cell line. This polyclonal knockout model provides a heterogeneous pool of gene-edited cells that collectively diminish CD36 function, enabling loss-of-function studies without clonal selection. The product serves as a versatile tool for investigating the multifaceted roles of CD36 in lipid metabolism, innate immunity, and cancer-related processes within a gastric epithelial context.
The AGS host cell line was originally derived from a human gastric adenocarcinoma and serves as a well-characterized model for gastric epithelial biology. These adherent epithelial cells retain key signaling pathways relevant to gastric mucosal function and carcinogenesis, making them particularly suitable for exploring the intersection of lipid uptake, inflammation, and tumor biology. The use of AGS cells allows researchers to study CD36-dependent mechanisms in a cellular environment that mirrors the gastric epithelium, facilitating translationally relevant discoveries in gastric pathophysiology.
CD36 functions as a multiligand scavenger receptor that is transcriptionally activated by PPAR??, PXR, and Nrf2 in response to ligands such as oxidized low-density lipoprotein (oxLDL) and long-chain fatty acids. Upon engagement, CD36 interacts with thrombospondin-1, caveolin-1, ??1 integrin, and CD9 to initiate downstream signaling cascades including NF-??B, MAPK, and PI3K/Akt pathways. These effectors drive foam cell formation, pro-inflammatory cytokine production, and thrombospondin-1-mediated responses. In innate immunity, CD36 recognizes pathogen-associated molecular patterns and facilitates phagocytosis, further linking lipid metabolism to immune surveillance.
In the gastric epithelial context, CD36 likely influences lipid handling, energy metabolism, and inflammatory responses that may contribute to gastric cancer progression. Given the emerging roles of lipid reprogramming in tumor aggressiveness, this knockout model enables dissection of CD36-driven metabolic and signaling adaptations in AGS cells. By ablating CD36, researchers can examine alterations in oxLDL uptake, fatty acid oxidation, and downstream activation of NF-??B and PI3K/Akt, which are pathways frequently dysregulated in gastric adenocarcinoma. This allows for a more nuanced understanding of how lipid scavenging receptors shape the gastric tumor microenvironment.
Typical experimental applications include lipid uptake assays to quantify fatty acid or oxLDL internalization, western blotting and flow cytometry to confirm CD36 loss, and functional studies like cell migration assays to assess phenotypic consequences. This polyclonal knockout population is also amenable to inflammatory cytokine ELISAs and fatty acid oxidation measurements, providing a comprehensive platform for metabolic disease, cardiovascular, and cancer research. For detailed product information and technical support, please contact Ascent Research.
