ACOT7 Knockout Jurkat Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population designed for functional dissection of the ACOT7 gene in a human T lymphocyte background. This model enables investigation of acyl-CoA thioesterase 7 (ACOT7) within the context of T cell biology, with the polyclonal format offering a representative spectrum of gene disruptions. Researchers can employ this system to examine ACOT7 roles in fatty acid metabolism, peroxisomal lipid homeostasis, and downstream signaling processes. It is particularly suited for biochemical, metabolic, and immunological assays requiring mass populations of edited cells.
The Jurkat cell line, derived from a human CD4+ T cell leukemia, is a widely used model for T cell activation, apoptosis, and signal transduction. These cells retain key features of primary T lymphocytes, including CD4 and TCR signaling machinery, facilitating investigations into MAPK, NF-??B, and NFAT pathways. Their rapid growth, genetic tractability, and well-defined signaling networks have established Jurkat as a cornerstone in immunological research and drug discovery targeting immune cell functions.
ACOT7 functions as a peroxisomal and cytosolic acyl-CoA thioesterase, hydrolyzing medium- and long-chain fatty acyl-CoAs to free fatty acids and coenzyme A (CoA). This enzymatic step modulates intracellular acyl-CoA pools, impacting fatty acid ??-oxidation, peroxisomal lipid metabolism, and PPAR signaling. ACOT7 is transcriptionally regulated by PPAR?? and PPAR?? and is responsive to fatty acids and insulin, situating it at a critical metabolic interface. Its products??free fatty acids and CoA??serve as metabolic substrates and signaling molecules, influencing PPAR activity and mitochondrial oxidation. Interacting with peroxisomal pathway components including ACOX1 and L-PBE, ACOT7 disruption provides a means to interrogate lipid flux and energy homeostasis.
Within Jurkat T lymphocytes, ACOT7-mediated fatty acid metabolism may critically shape T cell activation, proliferation, and effector functions. Activation entails metabolic reprogramming reliant on fatty acid oxidation, and ACOT7 could modulate the availability of lipid fuels and signaling mediators. This knockout model permits exploration of metabolic checkpoints that influence immune cell fate and function. Furthermore, the association of ACOT7 with obesity, type 2 diabetes, and metabolic syndrome positions these cells for studies bridging immunometabolism and systemic metabolic disease.
Research applications encompass functional genomics validation by RT-qPCR and western blotting, and phenotypic assessment of T cell activation markers via flow cytometry. Metabolic studies include fatty acid oxidation assays, metabolic flux analysis, and lipidomics, while PPAR reporter assays gauge nuclear receptor activity. Co-immunoprecipitation can reveal ACOT7 interactions with peroxisomal biogenesis factors, and immunofluorescence enables localization studies. These polyclonal knockout cells are valuable for drug screening against metabolic targets in leukemia and for dissecting lipid signaling in T cell immune responses. For further information, please contact Ascent Research.
