The CAT Knockout Jurkat Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population that disrupts the CAT gene in the Jurkat human T lymphocyte cell line. This loss-of-function model enables systematic investigation of catalase-dependent redox regulation in a well-characterized T-cell background. The polyclonal population preserves the heterogeneity inherent to CRISPR/Cas9-mediated gene disruption, providing a physiologically relevant system for studying oxidative stress responses without clonal selection artifacts.
Jurkat cells are an immortalized human T lymphocyte line originally derived from a 14-year-old male with acute T-cell leukemia. They retain key T-cell markers, including CD3, CD4, and the IL-2 receptor, and secrete IL-2 upon stimulation. This cell line is extensively employed in research on T-cell signaling, HIV infection, and leukemia biology, making it an ideal host for dissecting the role of catalase in immune cell redox homeostasis and transformation.
Catalase, encoded by the CAT gene, is the primary enzyme responsible for decomposing hydrogen peroxide into water and oxygen, thereby protecting cells from oxidative damage. Its expression is transcriptionally regulated by factors such as FoxO3a, NFE2L2 (Nrf2), and AP-1, which respond to stimuli including hydrogen peroxide, UV radiation, and TNF-alpha. Catalase interacts with peroxisomal import receptor PEX5, chaperone Hsp70, and components of the NADPH oxidase complex, and it functionally cooperates with superoxide dismutase (SOD1/SOD2), glutathione peroxidase, peroxiredoxins, and the thioredoxin system. Downstream, catalase activity modulates the MAPK pathway (ERK, JNK, p38), NF-??B, p53, and BCL2 family proteins, thereby influencing cell survival and proliferation. In the knockout model, loss of catalase elevates intracellular reactive oxygen species, dysregulating these redox-sensitive signaling networks.
In Jurkat T cells, redox balance is tightly coupled to T-cell receptor signaling, cytokine production, and apoptosis thresholds. CAT knockout therefore provides a powerful tool to examine how oxidative stress impacts T-cell activation, proliferation, and death. The model is particularly relevant for studying the intersection of redox biology and immune function in contexts such as leukemia, HIV-associated oxidative stress, and T-cell-mediated inflammation. By eliminating catalase activity, researchers can dissect the contributions of hydrogen peroxide and downstream effectors to T-cell fate decisions.
This polyclonal knockout cell population is suitable for diverse experimental applications, including oxidative stress mechanism studies, antioxidant compound screening, and apoptosis sensitivity assays following hydrogen peroxide challenge. Standard readouts include ROS detection via DCFDA or MitoSOX fluorescence, flow cytometric analysis of T-cell activation markers CD69 and CD25, Western blotting for catalase and pathway components, RT-qPCR for CAT mRNA, RNA-seq transcriptome profiling, and phospho-ERK/phospho-p38/NF-??B luciferase reporter assays. The model supports comprehensive investigations into redox signaling and its pathological consequences in T cells. For further technical information or ordering inquiries, please contact Ascent Research.
