The NSDHL Knockout Raji Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Raji B lymphoblast line, engineered for targeted disruption of the NSDHL gene. This product provides a heterogeneous pool of edited cells with loss-of-function mutations at the NSDHL locus, offering a versatile model for studying cholesterol biosynthesis and its implications in B cell biology without requiring single-cell clonal isolation.
The host Raji cell line is a well-characterized human Burkitt lymphoma-derived B lymphoblast line that maintains an EBV-positive status and expresses hallmark B cell markers such as CD19, CD20, and CD22. Widely utilized in immunological studies, EBV latency research, and cancer biology, Raji cells exhibit lymphoblastoid morphology and robust proliferative capacity, making them a reliable platform for genetic perturbation experiments. Their B lymphocyte origin renders them particularly suitable for examining the intersection of cholesterol metabolism and lymphoma pathogenesis.
NSDHL encodes an NAD(P)-dependent 3-beta-hydroxysteroid dehydrogenase that catalyzes the oxidative decarboxylation of C4-methylsterol intermediates in the post-squalene cholesterol biosynthetic pathway. Functioning downstream of SC4MOL and upstream of EBP, NSDHL is a critical enzyme in the conversion of 4-methylzymosterol to zymosterol. The gene’s expression is transcriptionally regulated by SREBF1 and SREBF2, master regulators of lipid homeostasis. Within the pathway, NSDHL operates in concert with HMGCR, SQLE, LSS, CYP51A1, SC5D, DHCR7, and DHCR24 to ensure proper sterol production. Disruption of NSDHL consequently alters the levels of downstream cholesterol intermediates, perturbing the entire cascade.
In the context of Raji B lymphoblasts, NSDHL knockout exerts a profound impact on cellular cholesterol homeostasis, likely modifying membrane lipid composition and lipid raft integrity. Given the dependence of B cell receptor signaling and EBV-associated proteins on membrane microdomains, loss of NSDHL may impair proliferative signals and survival pathways integral to lymphoma biology. This perturbation establishes a relevant model to dissect the role of cholesterol biosynthesis in B cell malignancies and to assess synthetic lethal interactions or metabolic vulnerabilities arising from sterol depletion.
The NSDHL Knockout Raji Polyclonal Cells are suitable for diverse research applications, including mechanistic studies of cholesterol metabolism, in vitro modeling of CHILD syndrome, and screening of inhibitors targeting sterol biosynthetic enzymes. Researchers can employ lipidomics and cholesterol quantification to profile sterol intermediates, RT-qPCR and immunoblotting to validate gene and protein expression changes, and flow cytometry to analyze membrane lipid composition. Proliferation and viability assays further enable functional readouts of pathway disruption. For further information or to request custom configurations, please contact Ascent Research.
