The ABHD16A Knockout SK-HEP-1 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human SK-HEP-1 hepatic adenocarcinoma line. This product provides a loss-of-function model for the ABHD16A gene, which encodes a serine hydrolase with phosphatidylserine (PS) lipase activity. The polyclonal population retains genetic heterogeneity, offering a robust system for investigating ABHD16A function without clonal selection bias. This knockout model is suitable for studies in lipid signaling, inflammation, and liver cancer biology.
The host cell line, SK-HEP-1, was originally isolated from the ascites of a patient with liver adenocarcinoma. These cells exhibit a unique dual phenotype, displaying both epithelial and endothelial characteristics, making them a valuable model for hepatic adenocarcinoma with endothelial-like properties. SK-HEP-1 cells are widely employed in research on liver disease, inflammation, and tumor biology, particularly for examining interactions between cancer cells and the microenvironment. Their hybrid nature allows for the study of processes such as angiogenesis, metastasis, and inflammatory responses within the liver context.
ABHD16A functions as a PS lipase, catalyzing the production of lysophosphatidylserine (lyso-PS), a bioactive lipid mediator. Lyso-PS signals through the GPR34 receptor to regulate inflammatory responses. The enzyme is activated by upstream stimuli including bacterial lipopolysaccharide (LPS) and tumor necrosis factor alpha (TNF??), and its expression is modulated by PPAR??. ABHD16A works in concert with ABHD12, a co-regulator of lyso-PS levels, to maintain lipid homeostasis. Downstream effects of lyso-PS include stimulation of pro-inflammatory cytokines such as interleukin-6 (IL-6) and TNF??, and promotion of macrophage polarization, thereby influencing immune cell function.
In the SK-HEP-1 context, disruption of ABHD16A eliminates lyso-PS generation, thereby interrupting GPR34-mediated signaling. This provides a powerful tool to dissect the specific contributions of lyso-PS to inflammatory and metabolic pathways in liver adenocarcinoma. The polyclonal knockout cells mirror the heterogeneous nature of tumor populations, enabling the study of ABHD16A’s role in cellular processes such as migration, invasion, and cytokine secretion. Given the dual epithelial-endothelial phenotype, this model is particularly relevant for exploring crosstalk between lipid signaling and angiogenesis in liver cancer.
Researchers can employ this knockout model in a variety of applications, including the investigation of lipid-mediated signaling in inflammation, validation of drug targets for inflammatory disorders, and studies on metabolic diseases such as obesity. Representative assays include RT-qPCR for cytokine expression, ELISA for secreted IL-6 and TNF??, lipidomics to quantify lyso-PS levels, flow cytometry for macrophage polarization markers, and GPR34 receptor activation assays. The polyclonal population is also suitable for cell migration and invasion studies. For additional product details, please contact Ascent Research.
