The B4GALT7 Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the SK-HEP-1 human hepatic adenocarcinoma cell line, with targeted disruption of the B4GALT7 gene. This polyclonal format preserves population heterogeneity and provides a robust loss-of-function model for studying B4GALT7-dependent glycosaminoglycan biosynthesis and proteoglycan function.
SK-HEP-1 is an epithelial-like cell line established from the ascitic fluid of a patient with liver adenocarcinoma. It exhibits endothelial characteristics and is widely employed as a model for liver sinusoidal endothelial cells and for studying hepatic tumor angiogenesis, metastasis, and cell-extracellular matrix interactions.
B4GALT7 encodes a galactosyltransferase that catalyzes the transfer of galactose to xylose in the tetrasaccharide linker region, a critical step in heparan sulfate and chondroitin sulfate biosynthesis. It functions downstream of xylosyltransferases, interacts with B3GALT6 and core proteins, and is regulated by TGFB1, PDGF, and SP1. Downstream, the pathway proceeds through B3GAT3 and the EXT1/EXT2 copolymerase to produce mature proteoglycans, including syndecans and glypicans. Knockout of B4GALT7 therefore disrupts the synthesis of sulfated glycosaminoglycans, impairing proteoglycan-dependent signaling and extracellular matrix integrity.
In SK-HEP-1 cells, loss of B4GALT7 creates a disease-relevant model to dissect the contribution of proteoglycans to hepatic adenocarcinoma behavior and liver endothelial function. The knockout allows interrogation of how defective glycosaminoglycan synthesis affects migration, invasion, and adhesion, and mimics molecular features of Ehlers-Danlos syndrome progeroid type, enabling study of skeletal dysplasia and joint hypermobility within a liver cancer context. The SK-HEP-1 B4GALT7 knockout model thus provides a versatile platform for exploring proteoglycan-mediated signaling pathways driven by growth factors such as TGF-?? and PDGF, and for assessing therapeutic interventions targeting glycosaminoglycan metabolism in liver cancer.
Applications include western blotting for proteoglycan core proteins, HPLC-based glycosaminoglycan disaccharide analysis, immunofluorescence for heparan sulfate localization, migration/invasion assays, RT-qPCR, and flow cytometry. Researchers can utilize these cells to quantify changes in heparan sulfate and chondroitin sulfate content, monitor proteoglycan-dependent cell motility, and develop in vitro models of connective tissue disorders. These polyclonal knockout cells support research on proteoglycan function in cancer, glycosaminoglycan biology, and Ehlers-Danlos syndrome models. For further details, please contact Ascent Research.
