The NDST1 Knockout Raji Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population designed for loss-of-function studies of the NDST1 gene in a human B lymphocyte background. This product provides a heterogeneous pool of Raji cells harboring targeted disruption of the NDST1 locus, enabling researchers to investigate the functional consequences of NDST1 ablation without the need for clonal isolation.
Raji cells are a well-established human Burkitt??s lymphoma B lymphocyte line that is positive for Epstein-Barr virus (EBV). These cells retain key B cell features, including the capacity for antibody production and antigen presentation, and are widely employed in immunological and oncological research. Their EBV status makes them particularly valuable for studying viral latency, lymphomagenesis, and immune evasion mechanisms.
NDST1 encodes the bifunctional enzyme N-deacetylase/N-sulfotransferase-1, which catalyzes the essential initial modification of heparan sulfate (HS) chains by removing N-acetyl groups and adding N-sulfate groups to glucosamine residues. This activity generates sulfation patterns that dictate HS interactions with a broad array of ligands, including growth factors such as FGF2 and VEGF, chemokines like CXCL12, and morphogens such as BMPs. NDST1 activity is regulated by upstream signals including NF-??B, TGF-??1, IL-1, and FGF2, and it controls downstream effectors such as ERK1/2, AKT, SMADs, and NF-??B. NDST1 functions within a biosynthetic complex containing EXT1, EXT2, and other modifying enzymes (NDST2, HS2ST, HS6ST), ultimately shaping HS-dependent signaling through FGF/FGFR, VEGF/VEGFR2, TGF-??/SMAD, and CXCL12/CXCR4 pathways.
In the Raji B cell context, heparan sulfate proteoglycans (HSPGs) are involved in cell adhesion, migration, and the regulation of immune responses. Disruption of NDST1 in this lymphoma line is anticipated to perturb HS sulfation profiles, thereby altering the binding and signaling of growth factors and cytokines critical for B cell survival, proliferation, and interaction with the tumor microenvironment. This model offers a relevant system to examine how defective HS modification influences lymphoma cell biology, including responses to chemokine gradients and angiogenic signals.
These polyclonal knockout cells are suitable for a range of applications, including B cell signaling studies, heparan sulfate function in lymphomas, and cancer microenvironment interactions. Researchers can employ this model in assays such as heparan sulfate profiling by mass spectrometry, western blotting for phosphorylated ERK and AKT, flow cytometry with anti-HS antibodies, and RT-qPCR for target gene expression. Functional studies may encompass cell proliferation, migration, and invasion assays, as well as FGF2 binding and antithrombin III activity measurements. Additionally, the cells can be utilized in drug sensitivity screens to evaluate compounds targeting HS modification or downstream pathways. For further information or custom requests, please contact Ascent Research.
