The CES3 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population featuring targeted disruption of the CES3 gene in Raji B lymphocytes. This heterogeneous cell pool, generated by gene editing, avoids clonal bias and captures diverse loss-of-function alleles. Cas9-mediated editing permanently abolishes CES3 carboxylesterase activity, providing a defined model to study ester-containing drug metabolism without pharmacological intervention.
Raji cells, derived from a Burkitt’s lymphoma patient, model mature B lymphocytes with retained antigen presentation and antibody production capacity. Widely employed in immunology and oncology, these cells are genetically tractable and endogenously express drug-metabolizing enzymes. Their lymphoma origin offers a clinically relevant platform for probing chemotherapeutic responses. Knocking out CES3 in Raji cells removes a critical ester-hydrolyzing function, allowing dissection of its role in drug sensitivity and cellular metabolism within a malignant B-cell context.
CES3 encodes a carboxylesterase responsible for hydrolyzing ester bonds in therapeutic agents and endogenous lipids, thereby modulating their activity and clearance. Its transcription is governed by nuclear receptors PXR (NR1I2), CAR (NR1I3), and PPAR??, which integrate xenobiotic and metabolic cues. In the endoplasmic reticulum, CES3 maturation involves interactions with ER retention proteins, protein disulfide isomerase, and molecular chaperones. The enzyme generates drug and lipid metabolites and functions within a network including CYP3A4, CES1, ABCB1, and UGT1A1. Disabling CES3 disrupts this pathway, enabling precise functional analysis.
Within Raji B lymphocytes, CES3 influences sensitivity to ester-containing chemotherapeutics and lipid signaling. Its knockout creates a clean loss-of-function background to study esterase-dependent drug metabolism separately from other resistance mechanisms. Given Burkitt’s lymphoma’s reliance on MYC-driven proliferation, altered lipid hydrolysis may further impact membrane dynamics and B-cell receptor pathways. This model is thus instrumental for exploring how metabolic reprogramming contributes to drug resistance and tumor maintenance in an immune-cell framework.
Researchers can employ drug sensitivity assays (MTT, apoptosis), esterase activity tests, lipidomics, and RNA-seq to profile CES3-dependent phenotypes. Western blotting and RT-qPCR enable verification of knockout and expression changes in related factors like PXR and CAR. The polyclonal population is ideal for toxicology and prodrug activation studies. For technical support or to order these cells, please contact Ascent Research.
