The ACY1 Knouckout Jurkat Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Jurkat human T lymphocyte cell line, engineered to disrupt the ACY1 gene encoding aminoacylase-1. This product is provided as a heterogeneous pool of edited cells, enabling population-level functional studies without clonal selection. The CRISPR/Cas9-mediated gene disruption results in loss of ACY1 catalytic activity, creating a reliable knockout model for investigating N-acetylated amino acid metabolism in a T lymphocyte background.
The Jurkat cell line is an immortalized human T lymphocyte leukemia cell line established from a patient with T cell leukemia. Widely employed in immunology and cancer research, Jurkat cells serve as a robust platform for examining T cell signaling, activation, and leukemogenesis. Their rapid proliferation and well-characterized signaling networks, including those involving T cell receptor-mediated pathways, make them ideal for metabolic studies and high-throughput functional assays.
The ACY1 gene encodes aminoacylase-1, a cytosolic zinc-dependent enzyme that catalyzes the hydrolysis of N-acetylated amino acids to liberate free amino acids and acetate. This reaction is integral to amino acid recycling and metabolism, contributing to the urea cycle and cellular energy homeostasis. ACY1 expression is transcriptionally regulated by the SP1 transcription factor and the NF-Y complex, and its enzymatic activity requires zinc as an essential cofactor. Inactivation of ACY1 disrupts the deacetylation of substrates such as N-acetylglutamate and N-acetylaspartate, leading to altered intracellular amino acid pools and reduced acetate production, which may impact energy metabolism and protein synthesis.
In the context of Jurkat T cells, ACY1 knockout offers a powerful tool for dissecting the role of amino acid metabolism in T lymphocyte function and leukemogenesis. Given the high metabolic demands of proliferating leukemia cells, impairment of amino acid recycling may affect cell growth, survival, and signal transduction. This model enables investigation of how acetate availability influences histone acetylation, gene expression, and T cell activation. Furthermore, it provides a relevant system for studying aminoacylase 1 deficiency and associated metabolic disorders, potentially bridging gaps in understanding between amino acid metabolism and immune cell pathology.
Researchers can employ these polyclonal knockout cells in diverse assays, including Western blotting and RT-qPCR to confirm loss of ACY1 expression, aminoacylase activity assays to verify functional knockout, and LC-MS-based metabolomics to profile changes in N-acetylated amino acids and downstream metabolites. Cell proliferation assays and acetate quantification can further elucidate metabolic consequences. This product is suited for metabolic studies in leukemia, aminoacylase deficiency modeling, drug discovery targeting amino acid metabolism, and T cell metabolism research. For technical inquiries or ordering information, please contact Ascent Research.
