The CD300LD Knockout AGS Polyclonal Cells product provides a heterogeneous population of AGS human gastric epithelial cells in which the gene encoding CD300LD has been disrupted via CRISPR/Cas9-mediated gene editing. This polyclonal knockout cell reagent serves as a versatile loss-of-function model to investigate the inhibitory immunoreceptor functions of CD300LD in a gastric adenocarcinoma background.
The AGS host cell line is a well-characterized human gastric adenocarcinoma epithelial line originally derived from a patient with stomach cancer. Widely employed as an in vitro model of gastric cancer, AGS cells are extensively used to study tumor cell proliferation, invasion, signaling pathway dysregulation, and pharmacological responses. Their gastric epithelial origin and tumorigenic properties make them particularly relevant for investigating mechanisms of immune evasion and inflammatory signaling within the gastric mucosa.
CD300LD is a type I transmembrane protein belonging to the CD300 family of immunoregulatory receptors and contains an immunoreceptor tyrosine-based inhibitory motif (ITIM) within its cytoplasmic domain. Upon binding to ligands such as phosphatidylserine (PtdSer) exposed on the surface of apoptotic cells or activated immune cells, CD300LD undergoes phosphorylation and recruits the tyrosine phosphatases SHP-1 and SHP-2. These phosphatases dephosphorylate key signaling intermediates downstream of activating receptors, thereby suppressing the PI3K/AKT and NF-??B pathways. Consequently, CD300LD negatively regulates the production of pro-inflammatory cytokines including TNF-?? and IL-6, contributing to the dampening of immune cell activation and maintenance of peripheral tolerance.
In the context of gastric adenocarcinoma, CD300LD may participate in tumor?Cimmune interactions, as inhibitory immunoreceptors are often co-opted by cancer cells to escape immune surveillance. By disrupting CD300LD in AGS cells, researchers can explore how loss of negative immune regulation influences tumor cell?Cintrinsic signaling, cytokine secretion profiles, and crosstalk with immune components. This knockout model thus serves as a valuable tool for dissecting the contribution of CD300LD to gastric cancer immune evasion and for evaluating its potential as an immune checkpoint target in the inflammatory milieu of gastric tumors.
The CD300LD Knockout AGS Polyclonal Cells are ideally suited for a broad spectrum of functional assays, including western blotting and RT-qPCR to confirm loss of CD300LD expression, flow cytometry to assess surface receptor levels, and ELISA to quantify changes in cytokine secretion such as TNF-?? and IL-6. The cells can be employed in proliferation, migration, and invasion assays to examine the impact of CD300LD loss on tumor cell behavior. Phospho-signaling analyses allow monitoring of PI3K/AKT and NF-??B pathway activity, while immune cell co-culture experiments enable the study of CD300LD-dependent regulation of immune evasion. For additional details or technical support, please contact Ascent Research.
