The KYAT3 Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed for loss-of-function studies of the KYAT3 gene. Derived from the near-haploid HAP1 cell line, this product provides a heterogeneous pool of cells with CRISPR/Cas9-mediated disruptions at the KYAT3 locus. The polyclonal format avoids clonal artifacts and is well-suited for population-based assays and genetic screens where robust gene inactivation is required.
HAP1 is a near-haploid human cell line derived from KBM-7 chronic myeloid leukemia cells. Its near-haploid genome simplifies knockout interpretation and reduces allele complementation. With rapid growth and adherent morphology, HAP1 is widely used in CRISPR-based functional genomics, drug target validation, and high-throughput screening, providing a genetically clean background for studying KYAT3 function.
KYAT3 encodes a pyridoxal phosphate (PLP)-dependent transaminase that irreversibly converts kynurenine to kynurenic acid, a neuroactive metabolite. Kynurenic acid acts as an antagonist at NMDA receptors and GPR35 and modulates aryl hydrocarbon receptor (AHR) signaling. KYAT3 activity is regulated by substrate availability, AHR signaling, and corticosteroids. In the kynurenine pathway, tryptophan is first metabolized by IDO1 or TDO2 to kynurenine, which is then acted upon by KYAT3 and KYAT1. By controlling this branch point, KYAT3 balances neuroprotective and neurotoxic pathway outputs.
Disruption of KYAT3 in HAP1 cells abrogates kynurenic acid production, redirecting kynurenine pathway flux. This mimics pathological states seen in Huntington??s disease and schizophrenia, where altered kynurenic acid levels are implicated. The near-haploid background ensures a clear phenotype, making this polyclonal knockout model ideal for dissecting KYAT3-dependent signaling pathways and screening for modulators of pathway activity.
Researchers can employ these cells for LC-MS?Cbased metabolite profiling of the kynurenine pathway, Western blotting for KYAT3 ablation, and cell viability assays under perturbed tryptophan metabolism. The polyclonal knockout cells support genetic interaction screens with IDO1, TDO2, or KYAT1 and neuroprotection studies targeting NMDA receptor or GPR35 signaling. This model enables therapeutic exploration of kynurenine pathway imbalances. For further details, please contact Ascent Research.
