The CD300LD Knockout SK-HEP-1 Polyclonal Cells product comprises a CRISPR/Cas9-edited polyclonal population of SK-HEP-1 cells carrying targeted disruption of the CD300LD gene. This knockout model provides a loss-of-function platform for studying CD300LD-dependent regulatory mechanisms in liver sinusoidal endothelial cells. The polyclonal format preserves cellular heterogeneity while abolishing CD300LD expression, enabling functional studies in a mixed genetic background that recapitulates native variability.
The SK-HEP-1 cell line originated from the ascites of a patient with liver adenocarcinoma and is widely employed as an in vitro model of hepatic sinusoidal endothelial cells. These cells exhibit characteristics of liver sinusoidal endothelium, including the ability to mediate filtration, endocytosis, and support leukocyte adhesion and transmigration. Their phenotypic features make them valuable for investigating liver-specific endothelial biology and disease-associated vascular alterations.
CD300LD is an inhibitory immune receptor that contains immunoreceptor tyrosine-based inhibitory motifs (ITIMs). Ligand engagement triggers recruitment of tyrosine phosphatases SHP-1 and SHP-2, which in turn dephosphorylate key signaling intermediates to suppress NF-??B and MAPK pathway activation. This cascade attenuates pro-inflammatory cytokine production and modulates immune cell responsiveness. CD300LD expression is regulated by factors such as IL-4, IL-10, and Toll-like receptor (TLR) ligands, positioning it at the intersection of cytokine and pathogen-sensing networks. Its interactions with SHP-1, SHP-2, and SHIP phosphatases are central to its role in maintaining immune homeostasis.
In liver sinusoidal endothelial cells, CD300LD functions as a gatekeeper of inflammatory signaling, fine-tuning responses to cytokines and microbial products that abound in the hepatic microenvironment. Knockout of CD300LD in SK-HEP-1 cells removes this inhibitory checkpoint, providing a powerful tool to dissect how loss of CD300LD impacts endothelial barrier integrity, cytokine secretion, and the capacity to support leukocyte adhesion and transmigration. This model is invaluable for exploring how dysregulated immune inhibitory signaling contributes to liver inflammation, fibrosis, and tumorigenesis.
Researchers can employ these CD300LD knockout SK-HEP-1 polyclonal cells in a broad array of functional analyses, including flow cytometric assessment of knockout efficiency, Western blot and RT-qPCR to confirm loss of protein and transcript, and cytokine secretion assays to quantify alterations in inflammatory output. Leukocyte adhesion assays and barrier integrity measurements are particularly relevant for evaluating how CD300LD influences endothelial-immune cell interactions and vascular permeability. These applications extend to liver cancer microenvironment studies, drug toxicity screens, and investigations of autoimmune and inflammatory liver diseases. For further details, please contact Ascent Research.
