ACYP1 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the Jurkat human T lymphocyte line, featuring targeted disruption of the ACYP1 gene. This heterogeneous pool provides a loss-of-function model without clonal selection, preserving biological variability relevant to T-cell leukemia research. The product is supplied as cryopreserved polyclonal knockout cells, validated for target gene disruption and typical Jurkat growth characteristics.
Jurkat cells are an immortalized T-cell line isolated from a pediatric acute T-cell leukemia patient. They are widely used as a model for T-cell receptor (TCR) signaling, apoptosis, and leukemogenesis. These cells express early T-cell markers and respond robustly to activation stimuli, making them ideal for functional genomic studies. Their well-characterized genome and ease of manipulation establish Jurkat as a standard platform for hematological malignancy research and drug discovery.
ACYP1 encodes acylphosphatase 1, which hydrolyzes acylphosphate intermediates on the Na+/K+-ATPase and Ca2+-ATPase (SERCA), thereby regulating ion pump activity and intracellular ion homeostasis. Its expression is governed by upstream signals including TCR activation, HIF1A under hypoxia, p53, and NRF2 in oxidative stress. ACYP1 activity influences glycolysis through modulation of phosphofructokinase and pyruvate kinase M2, and pyrimidine metabolism via carbamoyl phosphate synthetase II. Knockout of ACYP1 leads to accumulation of phosphorylated acyl groups on ATPases, impairing pump function, disrupting ion gradients, and perturbing glycolytic flux and nucleotide synthesis. In Jurkat cells, this results in defective TCR-mediated activation and compromised redox balance.
In Jurkat cells, ACYP1 deletion disrupts the metabolic adaptations required for T-cell activation and leukemic proliferation. The knockout phenotype combines impaired oxidative phosphorylation and glycolysis with direct ion pump inhibition, triggering apoptosis under metabolic stress. This model mirrors aspects of T-ALL where metabolic flexibility sustains malignancy, and it sensitizes cells to oxidative damage. Thus, these knockout cells are instrumental for studying the intersection of acylphosphatase function, T-cell metabolism, and leukemia progression.
These polyclonal knockout cells enable investigation of TCR signaling by flow cytometry (CD69, IL-2), proliferation (CFSE), and apoptosis (Annexin V) assays. Metabolomic profiling of pyrimidine intermediates and Na+/K+-ATPase activity measurements provide direct readouts of ACYP1 function. The cells are suitable for metabolic inhibitor screening, cancer metabolism studies, and T-ALL target validation. For further information on culture protocols or collaborative inquiries, please contact Ascent Research.
