The GSR knockout Jurkat polyclonal cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Jurkat human T lymphoblast cell line. This product provides a heterogeneous pool of cells with disrupted GSR expression, serving as a loss-of-function model for glutathione-disulfide reductase. The polyclonal format preserves editing diversity and is suitable for bulk functional assays that do not require clonal homogeneity.
Jurkat cells are a suspension lymphoblast line originating from a patient with acute T cell leukemia, widely used to model T cell signaling and leukemogenesis. Their rapid growth in culture and well-characterized signaling pathways make them an ideal host for studying redox biology in the context of malignant T lymphocytes. This background provides disease relevance for acute lymphoblastic leukemia research.
GSR encodes glutathione-disulfide reductase, which catalyzes the NADPH-dependent reduction of oxidized glutathione (GSSG) to reduced glutathione (GSH). Transcriptionally regulated by NFE2L2 (NRF2) under the control of KEAP1, GSR is a key enzyme in maintaining the GSH/GSSG balance. Downstream, GSH serves as a cofactor for GPX4 in neutralizing lipid peroxides, thereby inhibiting ferroptosis. GSR disruption impairs this antioxidant cascade, causing ROS accumulation and sensitizing cells to oxidative stress-induced death. The pathway also involves GCLC, GCLM, GSS, and SLC7A11.
In Jurkat T lymphoblasts, GSR knockout cripples the glutathione antioxidant system, mirroring hemolytic anemia due to GSR deficiency and highlighting redox vulnerability in leukemia. This model allows dissection of how drug-resistant cancers exploit glutathione metabolism and how T cell activation and proliferation are affected by redox imbalance. It provides a platform for mechanistic studies of ferroptosis in hematological malignancies.
Applications include examining redox control of T cell function, ferroptosis susceptibility in leukemia, and screening for glutathione reductase inhibitors. Typical assays are Western blotting for GSR and NRF2, GSH/GSSG ratio measurements, ROS detection by flow cytometry, and cell viability under oxidative challenge or ferroptosis induction. NRF2 reporter assays and inhibitor combination studies are also enabled. For technical inquiries, please contact Ascent Research.
