The B3GALT6 Knockout SK-HEP-1 Polyclonal Cells product is a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human SK-HEP-1 cell line, in which the B3GALT6 gene has been disrupted via targeted genome editing. This polyclonal pool captures a heterogeneous spectrum of gene-editing events, providing a functional population for loss-of-function studies without isolation of a single clonal isolate. The knockout model is designed to abolish the catalytic activity of the B3GALT6-encoded galactosyltransferase, enabling systematic investigation of glycosaminoglycan biosynthesis and its downstream cellular consequences in a well-characterized hepatic adenocarcinoma background.
SK-HEP-1 is a liver adenocarcinoma cell line originally established from the ascites of a patient, and it displays a unique hybrid phenotype that includes endothelial-like properties alongside mesenchymal characteristics. These features make SK-HEP-1 a widely used model system for hepatic sinusoidal endothelium, particularly in studies of tumor microenvironment interactions, angiogenic sprouting, and cancer cell adhesion. The cell line expresses markers of both epithelial and endothelial lineages, allowing researchers to dissect cross-talk between tumor cells and the vascular niche in the liver.
B3GALT6 encodes a galactosyltransferase that catalyzes the addition of galactose to the tetrasaccharide linkage region of glycosaminoglycans, a critical step prerequisite for the polymerization of heparan sulfate and chondroitin sulfate chains. The enzyme functions downstream of B4GALT7 and upstream of B3GAT3, EXT1, EXT2, and various sulfotransferases such as NDST1 and HS2ST1. Its activity is regulated by upstream signals including TGF-?? signaling, SOX9, BMP2, and endoplasmic reticulum stress sensors ATF4 and XBP1. Disruption of B3GALT6 impairs the synthesis of mature heparan sulfate proteoglycans such as syndecans and glypicans, as well as chondroitin sulfate proteoglycans including aggrecan and versican. Consequently, multiple growth factor pathways dependent on proteoglycan co-receptors are compromised, including FGFR, Hedgehog, and Wnt signaling.
In the context of SK-HEP-1 cells, loss of B3GALT6 function is expected to severely alter the extracellular matrix organization and cell surface presentation of glycosaminoglycans, thereby impacting cell adhesion, migration, and endothelial-like tube formation. Given the cell line’s use as a surrogate for hepatic sinusoidal endothelium, this knockout model offers a unique tool to study how defective glycosaminoglycan synthesis influences tumor-induced angiogenesis, metastatic dissemination, and the structural integrity of the perivascular matrix. The model also provides a platform to investigate connective tissue disorder mechanisms, as B3GALT6 mutations are associated with Ehlers-Danlos syndrome spondylodysplastic type.
This polyclonal knockout cell population is suitable for a broad range of research applications, including Ehlers-Danlos syndrome disease modeling, glycosaminoglycan biosynthesis profiling, and tumor microenvironment analysis. Typical assays performed with these cells include western blotting for proteoglycans, HPLC disaccharide composition analysis, RT-qPCR of glycosyltransferase expression, immunofluorescence staining for heparan sulfate chains, flow cytometric detection of glycosaminoglycans, migration and invasion assays, endothelial tube formation experiments, and Alcian blue staining for sulfated glycans. For further details regarding product specifications or custom modifications, please contact Ascent Research.
