The ACOT13 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population with disruption of the ACOT13 gene, designed for studying mitochondrial acyl-CoA thioesterase 13 function in T lymphocyte biology. This polyclonal pool of Jurkat cells enables robust loss-of-function investigations without single-cell cloning, while retaining genetic heterogeneity suitable for assessing ACOT13-dependent phenotypes in a human T cell leukemia background.
Jurkat cells, an immortalized T lymphocyte line derived from acute T cell leukemia peripheral blood, are a canonical model for T cell signaling, apoptosis, and leukemia metabolism. Their defined signaling pathways and amenability to genetic editing make them an optimal host for interrogating gene function in malignant T cell contexts.
ACOT13 encodes a mitochondrial thioesterase that hydrolyzes short-chain fatty acyl-CoAs to free fatty acids and CoASH, thereby controlling mitochondrial fatty acid oxidation and lipid homeostasis. ACOT13 expression is regulated by PPAR?? and NRF2, and its activity influences CoA availability and downstream fatty acid oxidation. It functions within a pathway including CPT1A, ACOX1, ECHS1, and HADHA. Disruption of ACOT13 alters acyl-CoA/CoA balance, impacting oxidative metabolism and lipid signaling.
In Jurkat T cells, ACOT13 knockout likely perturbs mitochondrial lipid handling, compromising energy production and altering lipid signaling critical for proliferation and survival. As T cell activation and leukemogenesis involve metabolic reprogramming with increased fatty acid oxidation, this model is ideal for dissecting acyl-CoA thioesterase contributions to leukemia cell metabolism. The polyclonal format prevents clonal artifacts, facilitating metabolic vulnerability identification.
This product supports diverse investigations via functional assays: mitochondrial fatty acid oxidation and respiration by Seahorse XF, lipidomic profiling, CoA quantitation, apoptosis and proliferation measurements, and drug sensitivity testing (e.g., etomoxir). It is a versatile tool for exploring ACOT13 roles in T cell leukemia lipid metabolism and screening for therapeutic targets. For detailed support, contact Ascent Research.
