The ADO Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population targeting the ADO gene in Jurkat T lymphocytes. This heterogeneous pool enables loss-of-function studies without single-cell cloning. It serves as an in vitro model for investigating cysteamine dioxygenase (ADO) in redox regulation and sulfur amino acid metabolism in a leukemic T-cell context.
Jurkat cells, an immortalized human T lymphocyte line from acute T cell leukemia, are widely used in immunology and cancer research. They exhibit constitutive T-cell signaling, robust proliferation, and genetic tractability, making them ideal for CRISPR/Cas9-mediated gene disruption to dissect T-cell biology, apoptosis, and metabolic pathways.
ADO encodes an iron-dependent enzyme that oxidizes cysteamine to hypotaurine, a key step in taurine biosynthesis. ADO is transcriptionally regulated by ATF4 and NRF2 and depends on cysteine availability. Its downstream products include hypotaurine, taurine, and hydrogen sulfide, which feed into glutathione synthesis, thereby maintaining thiol homeostasis and antioxidant defenses. The enzyme requires Fe2+ as a cofactor and functions within the broader cysteine and methionine metabolism, interacting with CDO and CSAD and the taurine transporter.
In Jurkat cells, ADO loss likely disrupts hypotaurine and taurine production, altering redox balance and possibly increasing oxidative stress sensitivity. Given the metabolic demands of leukemic T cells, this model is relevant for studying how taurine metabolism influences T-cell survival, activation, and metabolic adaptation, and for probing compensatory changes in cysteine/glutathione metabolism.
These polyclonal knockout cells support a range of assays: western blotting and RT-qPCR for ADO expression, LC-MS for hypotaurine/taurine, ROS detection and flow cytometry for oxidative stress markers, and viability/apoptosis assays under oxidative challenge. Applications include exploring taurine metabolism in immune cells, sulfur amino acid pathways in T lymphocytes, and redox effects on leukemia cell fitness. Contact Ascent Research for more information.
