The B3GALT6 Knockout HeLa Polyclonal Cells product comprises a CRISPR/Cas9-edited polyclonal knockout cell population targeting the B3GALT6 gene in the human HeLa cell line. This loss-of-function model enables investigation of beta-1,3-galactosyltransferase 6 function in glycosaminoglycan biosynthesis and proteoglycan assembly, providing a versatile tool for glycobiology and extracellular matrix research.
Derived from HPV18-positive cervical adenocarcinoma, HeLa cells are a widely used immortalized epithelial cell line. Their extensive characterization, rapid growth, and genetic tractability make them an ideal host for studying cell-surface proteoglycan dynamics and ECM-related pathways in a cancerous context, offering physiologically relevant backgrounds for B3GALT6 knockout analyses.
B3GALT6 encodes beta-1,3-galactosyltransferase 6, a key enzyme that catalyzes galactose transfer to the tetrasaccharide linker during glycosaminoglycan chain initiation. It functions within the linker enzyme complex alongside B4GALT7, B3GAT3, and XYLT2, and is transcriptionally regulated by TGFB1, SP1, and GLI factors. Downstream, B3GALT6 activity is essential for the biosynthesis of heparan sulfate and chondroitin sulfate chains on proteoglycans such as aggrecan, decorin, and syndecan-1. Disruption of this enzyme leads to defective glycosaminoglycan elongation, compromising extracellular matrix organization and growth factor signaling.
In HeLa cells, B3GALT6 knockout disrupts proteoglycan-dependent processes including cell adhesion, migration, and ECM remodeling, which are frequently dysregulated in cancer progression. This model mirrors molecular defects observed in Ehlers-Danlos syndrome, spondylodysplastic type, where B3GALT6 mutations impair connective tissue integrity. The polyclonal nature of the knockout population captures heterogeneous responses to ECM disruption, enhancing translational relevance for studying tumor microenvironment dynamics and connective tissue disorders.
Typical research applications include Western blotting and RT-qPCR for knockout validation, HPLC-MS-based disaccharide analysis to assess glycosaminoglycan composition, and Alcian blue staining for proteoglycan visualization. Functional assays such as immunofluorescence, cell migration, and ECM adhesion assays further enable dissection of ECM?Ccell interactions. This model supports drug screening for connective tissue diseases and investigations into cancer ECM remodeling. For additional information, please contact Ascent Research.
