The LDLR Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited population from the Raji B lymphocyte line with targeted LDLR disruption. The heterogeneous knockout pool eliminates LDL receptor function, enabling analysis of endocytosis and cholesterol homeostasis without clonal bias. These polyclonal cells are suitable for diverse biochemical and genetic investigations of LDLR-dependent pathways in a human immune cell context.
The Raji cell line, originating from an Epstein-Barr virus-positive Burkitt lymphoma, is a widely used human B lymphocyte model. Raji cells retain key features of humoral immunity, including robust proliferation, antigen presentation, and antibody production capacity. This background allows researchers to examine lipid metabolism in the context of B cell biology and immune function.
LDLR encodes a cell-surface receptor that internalizes low-density lipoprotein via clathrin-mediated endocytosis. Upon binding APOB, the receptor?CLDL complex is endocytosed with the aid of LDLRAP1 and directed to lysosomes, releasing free cholesterol that represses SREBP2-driven transcription of cholesterol synthesis genes including HMGCR. PCSK9 post-translationally regulates LDLR abundance, and insulin potentiates receptor activity. In the knockout, loss of LDLR eliminates regulated LDL uptake, severing the cholesterol-sensing feedback loop.
In Raji B lymphocytes, LDLR knockout uncouples exogenous cholesterol acquisition from cellular metabolism, allowing dissection of receptor-mediated lipid import versus de novo synthesis. This is particularly relevant for studying cholesterol??s role in B cell activation, membrane dynamics, and antibody production. As a surrogate for familial hypercholesterolemia, these cells model loss-of-function LDLR mutations that drive cardiovascular disease, and they also permit investigation of lipid-linked oncogenic mechanisms in Burkitt lymphoma-derived B cells.
These polyclonal knockout cells are suited for fluorescent LDL uptake assays, cholesterol quantification, and viability testing under lipid deprivation. Western blotting, flow cytometry, and RT-qPCR enable validation of LDLR loss and profiling of SREBP2 targets. Transcriptomic analyses via RNA-seq reveal global metabolic rewiring. The population is ideal for high-throughput screening of LDLR upregulators and functional studies of PCSK9-mediated regulation. For further information, please contact Ascent Research.
