The PGRMC2 Knockout Raji Polyclonal Cells offer a genetically disrupted Raji B-lymphocyte cell population, engineered via CRISPR/Cas9 to ablate PGRMC2 function. This polyclonal knockout pool provides a tractable loss-of-function model within the established EBV-positive Burkitt??s lymphoma background, circumventing the need for single-cell cloning. The heterogeneous cell population is suited for pooled assays that reflect average gene disruption effects across the polyclonal population.
Raji cells, derived from an EBV-infected Burkitt??s lymphoma, are a cornerstone model in immunology and oncology, noted for their robust proliferation, antibody production, and antigen-presentation capacity. They already express key components of the heme and cholesterol pathways, including CYP51A1 and PPARgamma, making them intrinsically appropriate for dissecting PGRMC2-related metabolic functions.
PGRMC2 (progesterone receptor membrane component 2) is a heme-binding membrane protein that directly interacts with and stabilizes CYP51A1, a lanosterol 14-??-demethylase crucial for cholesterol biosynthesis. It also serves as a co-regulator of PPARgamma, amplifying the expression of adipogenic and lipogenic target genes such as FASN and SCD1. PGRMC2 expression is driven by PPARgamma and C/EBPalpha and is modulated by upstream signals from insulin, progesterone, and heme. Consequently, PGRMC2 integrates heme availability with cholesterol synthesis and PPARgamma-driven transcriptional responses, influencing lipid homeostasis and insulin sensitivity. In the knockout Raji cells, loss of PGRMC2 is expected to destabilize CYP51A1, reduce cholesterol production, and attenuate PPARgamma target gene activation.
B-cell lymphomas, including Burkitt??s lymphoma, exhibit heightened metabolic demands to support rapid division. PGRMC2??s role at the nexus of heme sensing and lipid metabolism suggests it may be essential for supplying cholesterol and steroid intermediates required for membrane biogenesis and signaling. Disruption of PGRMC2 in Raji cells can therefore reveal metabolic dependencies and sensitization to lipid starvation or heme depletion. This model allows delineation of the crosstalk between heme-binding proteins, cytochrome P450 enzymes, and nuclear receptor signaling in a malignant B-cell context, with potential implications for understanding metabolic targets in lymphoma therapy.
Researchers can utilize these cells in a variety of experimental workflows. Western blotting and RT-qPCR serve to confirm PGRMC2 knockout and assess downstream effects on CYP51A1, FASN, and other metabolic regulators. Quantitative cholesterol and heme assays paired with proliferation or apoptosis measurements under metabolic stress conditions dissect functional consequences. Flow cytometry enables monitoring of B-cell surface markers, while RNA-seq and metabolomic profiling provide comprehensive views of transcriptomic and metabolic reprogramming. Together, these applications support studies in cancer metabolism, heme trafficking, steroid hormone signaling, and B-cell biology. For technical inquiries, please contact Ascent Research.
