The CYP1B1 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Raji B lymphocyte cell line, designed for targeted disruption of the CYP1B1 gene in a human Burkitt’s lymphoma background. This loss-of-function model eliminates CYP1B1 enzymatic activity without clonal selection, providing a heterogeneous pool of cells with targeted gene disruption suitable for studying gene function in a mixed population context. The polyclonal format retains the cellular diversity of the original Raji line while removing CYP1B1-dependent metabolic capabilities, enabling robust functional comparisons against wild-type controls.
Raji cells are an EBV-positive B lymphocyte line originating from a patient with Burkitt’s lymphoma, widely used in immunology and cancer research. These suspension cells express B-cell surface markers and exhibit key features of humoral immunity, including the capacity for antibody production and antigen presentation. The malignant B-cell background offers a relevant model for studying oncogenic signaling, lymphoid biology, and drug responses within the hematopoietic system. Raji cells maintain active metabolic and signaling pathways, making them a well-characterized host for gene-editing applications aimed at dissecting lymphocyte-specific functions.
CYP1B1 encodes a cytochrome P450 monooxygenase critical for the hydroxylation of diverse endogenous and xenobiotic substrates. It is transcriptionally activated by the aryl hydrocarbon receptor (AHR) upon exposure to ligands such as dioxin and is also regulated by estrogen receptor (ER) signaling, cAMP, and retinoic acid. CYP1B1 cooperates with NADPH-cytochrome P450 reductase (POR) and cytochrome b5 to catalyze the 4-hydroxylation of estradiol, generating catechol estrogens that can redox cycle to produce reactive oxygen species and form DNA adducts. This enzyme also bioactivates procarcinogens, contributing to genotoxic stress. Downstream targets include cell cycle regulators, and the pathway converges with detoxification systems such as COMT, GST, and NQO1, which further process the reactive metabolites.
In the Raji B-cell context, CYP1B1 knockout provides a unique tool to investigate estrogen catabolism, oxidative stress, and procarcinogen activation specifically within lymphocytes. The elimination of CYP1B1 activity allows researchers to assess its contribution to DNA damage, apoptosis, and metabolic reprogramming in a hematological cancer model. This system is particularly relevant for studying hormone-related malignancies and the role of B cells in the metabolism of steroid hormones and environmental carcinogens. By removing a key source of genotoxic metabolites, the knockout cells help clarify mechanisms of lymphomagenesis and cellular defense against oxidative insults.
Research applications include drug metabolism studies using LC-MS metabolite profiling, toxicological assays such as the EROD assay for CYP1 activity and comet assay for DNA damage, and functional analyses of estrogen signaling via Western blotting and RT-qPCR. The cells are also suited for cell viability (MTT) and apoptosis (flow cytometry) assays to evaluate drug sensitivity in hematological malignancies, as well as lipid peroxidation and immunocytochemistry studies. This model supports investigations into the interplay between CYP1B1 and pathways like AHR and estrogen signaling in a B-cell environment. For further details or to request a quotation, please contact Ascent Research.
