The MGST3 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population designed to disrupt the MGST3 gene in human Raji B lymphocytes, eliminating microsomal glutathione S-transferase 3 function. This model facilitates research into oxidative stress response, ferroptosis regulation, and cellular detoxification. Provided as a heterogeneous pool of edited cells in suspension culture, it captures the diversity of CRISPR-mediated gene disruption, avoiding clonal biases typical of single-cell-derived lines.
The Raji host cell line is an EBV-positive human B lymphoblastoid line originating from Burkitt??s lymphoma, offering a clinically relevant background for lymphoma and immunology studies. These suspension-adapted cells are widely used to investigate antibody production, immune signaling pathways, and cancer cell vulnerabilities, particularly in the context of oxidative stress and metabolic reprogramming inherent to malignant transformation.
MGST3 encodes a microsomal glutathione S-transferase that catalyzes the conjugation of reduced glutathione to electrophilic substrates and the reduction of lipid hydroperoxides, thereby safeguarding cellular membranes from oxidative insult. Transcriptionally controlled by NFE2L2 (NRF2) in response to oxidative stress and modulated by KEAP1, MGST3 interacts with glutathione and functionally cooperates with family members MGST1 and MGST2. It also engages with LTC4 synthase (LTC4S) and 5-lipoxygenase activating protein (ALOX5AP), acting as a critical component of the glutathione metabolism and ferroptosis defense network, where it works alongside GPX4 to suppress lipid peroxidation-driven cell death.
In the Raji B cell model, loss of MGST3 ablates a central antioxidant mechanism, rendering cells more sensitive to oxidative stress and ferroptotic triggers. Given the heightened metabolic activity and oxidative burden in Burkitt??s lymphoma, this knockout polyclonal population may unveil vulnerabilities exploitable by ferroptosis-inducing therapies. It thus provides a powerful system for dissecting the interplay between glutathione-dependent detoxification, redox homeostasis, and tumorigenic signaling, as well as for studying NRF2-mediated adaptive responses in lymphoid cancer.
Typical experimental uses encompass viability assays under oxidative challenge, lipid peroxidation detection with C11-BODIPY, intracellular glutathione measurement, western blotting for MGST3 and NRF2, and ROS monitoring by flow cytometry. RT-qPCR profiling of NRF2 target genes further elucidates downstream effects. The cells are particularly valuable for high-throughput screening of ferroptosis inducers and for probing the detoxification of xenobiotic electrophiles. For additional details or ordering inquiries, please contact Ascent Research.
