The HMOX1 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Jurkat human T lymphoblastoid cell line. This product features targeted disruption of the HMOX1 gene, producing a heterogeneous pool of cells with loss-of-function mutations that eliminate heme oxygenase-1 activity. The polyclonal format avoids clonal selection bias, offering a robust and representative model for investigating HMOX1-dependent processes in a T cell context.
Jurkat cells, originally isolated from the peripheral blood of a 14-year-old male with acute lymphoblastic leukemia, are a widely adopted model for T cell signaling and leukemia biology. These suspension cells grow rapidly and are amenable to high-throughput applications, providing a well-characterized platform for studying T cell activation, apoptosis, and cytokine production. Their lymphoid origin and oncogenic background make them particularly relevant for research intersecting immunology and cancer.
HMOX1 encodes heme oxygenase-1, the rate-limiting enzyme in heme catabolism that cleaves heme into biliverdin, carbon monoxide (CO), and free iron. These products mediate cytoprotective, antioxidant, and anti-inflammatory effects. HMOX1 expression is transcriptionally regulated by NFE2L2 (NRF2) and BACH1 competing for antioxidant response elements (AREs). NRF2, stabilized under oxidative stress, activates transcription, whereas BACH1 represses it. Additional regulators include HIF1A, AP-1 (JUN/FOS), IL-10, and TNF. Downstream, CO signals through guanylate cyclase and MAP kinase pathways, bilirubin scavenges free radicals, and ferritin sequesters iron. The enzyme requires NADPH-cytochrome P450 reductase as an electron donor and interacts directly with heme and BACH1.
Disruption of HMOX1 in Jurkat T cells abrogates this protective response, markedly increasing susceptibility to oxidative stress-induced apoptosis. This is critical given the high metabolic activity of leukemic T cells and their reliance on redox balance. Moreover, loss of HMOX1 can perturb T cell receptor signaling, as CO and bilirubin modulate NF-??B and MAPK cascades. Thus, this polyclonal knockout model enables dissection of the crosstalk between heme metabolism, iron homeostasis, and T cell function, while offering insights into mechanisms of cancer cell resilience.
These cells can be used to study NRF2-mediated oxidative stress responses, heme degradation, and iron handling in a T lymphoid background. Standard assays include western blotting and RT-qPCR for HMOX1, ROS detection, heme oxygenase activity assays, flow cytometric apoptosis analysis (Annexin V/PI), and immunofluorescence. They are also suitable for T cell activation assays (CD69 expression) and high-throughput screening of NRF2 pathway modulators. Additional applications include anti-inflammatory drug testing and cancer resilience studies. For detailed technical inquiries, please contact Ascent Research.
