The LDAH Knockout Raji Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population in which the LDAH gene has been disrupted through a targeted gene-editing approach. This loss-of-function model provides a powerful tool for studying the role of the lipid droplet-associated hydrolase LDAH in the context of human Burkitt lymphoma-derived B lymphocytes. The polyclonal nature of the knockout population preserves the genetic heterogeneity of the Raji cell line while ensuring robust disruption of the target gene across the cell pool, enabling reproducible phenotypic analyses without clonal selection artifacts.
Raji cells are a well-characterized human B lymphocyte line established from a patient with Burkitt lymphoma. They are Epstein-Barr virus (EBV) positive and grow in suspension, recapitulating key features of adaptive immune cells involved in antibody secretion. The Raji line is widely used in cancer biology, immunology, and virology research due to its transformed phenotype and defined signaling pathways. As a Burkitt lymphoma model, Raji cells exhibit deregulated cell-cycle progression and metabolic reprogramming, making them particularly suitable for investigating oncogenic processes and therapeutic interventions.
LDAH (lipid droplet-associated hydrolase) localizes to the surface of lipid droplets and catalyzes the hydrolysis of cholesterol esters, thereby modulating intracellular cholesterol and free fatty acid pools. Its activity is regulated by upstream factors such as the transcription factors PPAR?? and LXR, which control lipid metabolism genes in response to nutrient availability. LDAH functions within a network of lipid droplet-associated proteins, interacting with perilipin 1, CGI-58, and ATGL to coordinate the mobilization of neutral lipids. Disruption of LDAH disrupts the balance between cholesterol ester storage and release, altering lipid droplet composition and subsequent signaling events downstream of lipid-derived metabolites.
In the Raji B-cell context, knockout of LDAH profoundly affects lipid droplet turnover and cholesterol homeostasis, processes that are increasingly recognized as critical for malignant lymphocyte survival and proliferation. Aberrant cholesterol metabolism supports membrane biogenesis and provides signaling lipids necessary for B-cell receptor signaling and stress responses. The LDAH knock-out model therefore enables dissection of the metabolic dependencies that underlie Burkitt lymphoma growth. It also offers a platform to study how lipid droplet dynamics intersect with oncogenic pathways in EBV-transformed B cells, potentially revealing new vulnerabilities for therapeutic targeting.
This product is ideally suited for a wide range of applications in lipid droplet biology, cancer metabolism, and metabolic disease modeling. Researchers can employ Western blotting or RT-qPCR to confirm LDAH disruption, lipid droplet staining with BODIPY to visualize neutral lipid accumulation, and enzymatic assays to quantify cholesterol ester and triglyceride levels. Functional studies may include cell proliferation assays and metabolic flux analysis to assess the impact of LDAH loss on B-cell bioenergetics. The polyclonal knockout cells are also valuable for co-culture experiments, drug screening, and gene expression profiling. For further information or to discuss custom configurations, please contact Ascent Research.
