The KYNU Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population of human T lymphocytes with targeted disruption of the KYNU gene. This heterogeneous pool of knockout cells avoids clonal artifacts and provides a robust model for dissecting gene function within a mixed genetic background. The use of a polyclonal format facilitates the study of loss-of-function phenotypes while maintaining the biological variability inherent to T cell populations, making it suitable for investigations requiring population-level responses rather than clonal uniformity.
Jurkat cells serve as a widely adopted human T cell leukemia line and a cornerstone model for T cell receptor (TCR) signaling, apoptosis regulation, and HIV infection studies. Originating from an acute T cell leukemia patient, these cells retain key features of T lymphocyte biology, including the capacity to activate downstream signaling cascades upon TCR engagement. Their well-characterized signaling networks and ease of genetic manipulation make them an ideal host for CRISPR-mediated gene editing, enabling researchers to explore the molecular underpinnings of T cell function.
KYNU encodes kynureninase, a pyridoxal phosphate (PLP)-dependent enzyme that catalyzes the hydrolytic cleavage of L-kynurenine and 3-hydroxykynurenine to anthranilic acid and 3-hydroxyanthranilic acid, respectively. This reaction is a crucial branch point in the tryptophan degradation pathway, operating downstream of indoleamine 2,3-dioxygenase (IDO) and tryptophan 2,3-dioxygenase (TDO). Kynureninase activity is tightly regulated by inflammatory mediators such as interferon-gamma (IFNG), tumor necrosis factor (TNF), and interleukin-1 beta (IL1B), and is modulated by aryl hydrocarbon receptor (AhR) ligands. Through its production of 3-hydroxyanthranilic acid, KYNU feeds into the synthesis of quinolinic acid, picolinic acid, and ultimately NAD+, while also influencing levels of kynurenic acid??an AhR agonist. This places KYNU at the intersection of NAD+ biosynthesis and AhR-mediated transcriptional regulation.
In the Jurkat T cell context, KYNU disruption can profoundly alter tryptophan metabolite flux, potentially reducing NAD+ availability and modifying AhR signaling outputs. Given that T cell activation, proliferation, and apoptosis are metabolically demanding processes sensitive to intracellular NAD+ levels and AhR activity, this knockout model offers a powerful system to examine how kynureninase-dependent metabolism shapes lymphocyte behavior. It also provides a platform for studying the immunomodulatory roles of the kynurenine pathway in transformed T cells, with implications for cancer immune evasion and inflammatory disorders.
Typical research applications include LC-MS-based metabolite profiling to quantify tryptophan catabolites, NAD+/NADH ratio measurements under immune stimulation, kynureninase enzyme activity assays, and AhR reporter assays to evaluate signaling changes. These polyclonal cells are also valuable for TCR activation studies, cytokine production analysis, and apoptosis assays that probe how KYNU loss influences Jurkat functional responses. Co-culture experiments with tumor cells or antigen-presenting cells can extend utility into tumor immunology, while pharmacological inhibitor screens may identify compounds that modulate the pathway. For further details, technical support, or pricing inquiries, please contact Ascent Research.
