The ATOX1 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from Jurkat human T lymphocyte leukemia cells. This loss-of-function model disrupts the ATOX1 gene (Homo sapiens), eliminating its copper chaperone activity without clonal isolation. The heterogeneous pool allows pooled functional studies while avoiding clonal artifacts.
Jurkat cells, a suspension lymphoblast line from acute T-cell leukemia, serve as a standard model for T-cell receptor signaling, cytokine production, and immune function. They express CD3 and CD4 and produce interleukin-2 upon activation, making them ideal for research into adaptive immunity and leukemogenesis.
ATOX1 functions as a copper chaperone that specifically transfers copper to the ATPases ATP7A and ATP7B via direct protein-protein interactions. This delivery step is essential for maturation of secretory cuproenzymes like SOD3 and lysyl oxidase, thereby maintaining copper homeostasis and antioxidant defense. ATOX1 is regulated by copper ions, oxidative stress, and metal-responsive transcription factors, and it acts upstream of ATP7A/B in a pathway that includes the copper importer CTR1.
In Jurkat T cells, ATOX1 knockout enables dissection of copper??s role in immune signaling. Copper modulates TCR-driven activation, proliferation, and cytokine output, partly through cuproenzyme activity. By abolishing ATOX1, researchers can assess how copper trafficking defects affect SOD3-mediated ROS scavenging and lysyl oxidase function, linking to T-cell pathophysiology and leukemia. This model is relevant to Menkes disease, Wilson disease, cancer, and neurodegeneration.
Applications include studying copper homeostasis in T cells, oxidative stress responses, and copper-dependent immune signaling. Compatible assays: Western blot, RT-qPCR, copper uptake, SOD activity, ROS detection, and flow cytometry for proliferation. The polyclonal format suits pooled screens and drug testing. For support, contact Ascent Research.
