DSEL Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population in which the DSEL gene has been disrupted using CRISPR/Cas9 technology. This product provides a loss-of-function model in the HAP1 cell background, enabling researchers to investigate the role of DSEL in dermatan sulfate biosynthesis and glycosaminoglycan metabolism. The polyclonal nature of the knockout population ensures genetic heterogeneity, reflecting a pooled knockout effect rather than a clonal isolate.
HAP1 is a near-haploid human cell line derived from the KBM-7 chronic myeloid leukemia (CML) cell line. Its near-haploid karyotype simplifies genetic manipulation and phenotypic analysis, making it a widely used model for functional genomics and knockout studies. HAP1 cells retain key features of malignant myeloid cells, providing a relevant context for studying the role of extracellular matrix components in leukemia biology.
DSEL encodes a protein with sequence similarity to dermatan sulfate epimerase, which is predicted to catalyze the epimerization of D-glucuronic acid to L-iduronic acid within dermatan sulfate chains, a modification critical for the function of proteoglycans such as decorin (DCN) and biglycan (BGN). DSEL functions within the glycosaminoglycan biosynthesis pathway and is regulated by upstream factors including TGFB1, BMP2, and SOX9. It interacts with DSE, CHST14, CHST3, B4GALT7, and EXT1, and its activity influences downstream targets DCN, BGN, VCAN, and CSPG4.
Disruption of DSEL in HAP1 cells is expected to alter dermatan sulfate structure, impacting proteoglycan function and extracellular matrix organization. Given the role of proteoglycans in cell adhesion, migration, and signaling, this knockout model offers a tool to explore how dermatan sulfate modifications affect leukemia cell behavior. In CML, altered glycosaminoglycan profiles may contribute to aberrant cell?Cmatrix interactions, making HAP1 a suitable host for dissecting DSEL??s contributions.
This knockout cell population is suitable for a range of research applications, including investigation of dermatan sulfate biosynthesis, analysis of proteoglycan function in cancer, and study of glycosaminoglycan modifications in leukemia cell adhesion and migration. Representative experimental approaches include western blotting for decorin and biglycan, glycosaminoglycan disaccharide analysis by HPLC or mass spectrometry, immunofluorescence for dermatan sulfate epitopes, RT-qPCR for DSEL and related enzymes, cell adhesion and migration assays, and flow cytometry for cell surface proteoglycans. For further information, please contact Ascent Research.
