The NDST2 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited human polyclonal knockout cell population, derived from the Raji B lymphocyte cell line, with targeted disruption of the NDST2 gene. This product provides a loss-of-function model to study NDST2-dependent pathways in a B-cell background. Because the knockout is polyclonal, the cell population harbors a heterogeneous mix of NDST2 gene disruptions introduced by Cas9-mediated cleavage, reflecting the typical diversity of a non-clonal knockout pool.
Raji cells are an Epstein-Barr virus-positive, lymphoblastoid B lymphocyte line originally established from a Burkitt lymphoma patient. These suspension-adapted cells are widely employed as a model for B-cell biology, lymphomagenesis, and hematological malignancies. Their EBV-transformed status enables straightforward culture and genetic manipulation, while retaining key B-cell signaling and antigen-presentation machinery.
NDST2 encodes an N-deacetylase/N-sulfotransferase that catalyzes the initial modification of glucosamine residues within heparan sulfate chains, a pivotal step in heparin biosynthesis. This enzyme acts downstream of KIT receptor signaling, which is activated by stem cell factor (SCF), and is transcriptionally regulated by MITF and IL-3. NDST2 cooperates with the EXT1/EXT2 copolymerase complex and downstream sulfotransferases (HS2ST, HS6ST, HS3ST) to produce mature heparan sulfate proteoglycans. Once generated, heparin chains serve as a scaffold for granule-associated mediators in mast cells, such as histamine, mast cell proteases, and serglycin. NDST2 deficiency thus disrupts heparin production, compromising the storage of these effectors and attenuating mast cell degranulation downstream of high-affinity IgE receptor (Fc??RI) engagement.
Although NDST2 is conventionally recognized for its function in mast cells, its expression and role in B lymphocytes remain less characterized. By generating NDST2 knockout in Raji cells, researchers can explore the contribution of heparan sulfate modifications to B-cell lymphomagenesis, tumor microenvironment interactions, and glycan-mediated signaling. This model allows investigation of how the loss of NDST2-catalyzed sulfation alters growth factor presentation, such as FGF2 binding, and chemokine signaling networks, potentially affecting lymphoma cell proliferation, migration, and drug sensitivity.
This knockout cell pool is suited for a range of experimental applications, including RT-qPCR to assess changes in downstream targets, western blotting for heparan sulfate chain modifications, and flow cytometry to detect heparan sulfate epitope loss. Co-culture systems with mast cells can be established to examine mast cell?CB cell crosstalk in allergic inflammation or tumor microenvironments. Migration assays with chemokines and drug sensitivity profiling in lymphoma provide functional readouts of NDST2 loss. Collectively, the NDST2 Knockout Raji Polyclonal Cells serve as a useful tool for dissecting glycosaminoglycan biology in B-cell contexts. For technical inquiries, please contact Ascent Research.
