The ACSL1 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Jurkat T lymphoblast line, featuring targeted disruption of the ACSL1 gene. This pooled format provides a heterogeneous population of cells with loss-of-function mutations in ACSL1, generated by CRISPR/Cas9-mediated gene editing, enabling researchers to analyze the collective impact of ACSL1 ablation without clonal selection artifacts. The cells are supplied from a standard Jurkat host background and are suitable for in vitro studies of fatty acid metabolism, leukemia biology, and ferroptosis signaling.
Jurkat cells are a widely utilized human T lymphoblast model originating from a 14-year-old male with acute T cell leukemia. They display a mature T cell phenotype as CD3+ CD4+ CD8? cells and exhibit IL-2-independent growth while retaining functional T cell receptor (TCR) expression and intact downstream signaling machinery. This makes them a relevant platform for examining how metabolic reprogramming??such as altered fatty acid utilization??intersects with TCR-dependent pathways, proliferation, and leukemogenesis.
ACSL1 encodes long-chain acyl-CoA synthetase 1, a key enzyme that activates long-chain fatty acids to their acyl-CoA derivatives, committing them to either mitochondrial ??-oxidation for energy production or to complex lipid synthesis, including triglycerides and phospholipids. ACSL1 operates at a critical metabolic node downstream of transcription factors such as PPAR??, LXR, and SREBP1, and in response to insulin and glucose availability. It interacts with fatty acid transport proteins FATP1 and FATP4, and channels acyl-CoA toward downstream enzymes like CPT1A (carnitine palmitoyltransferase 1A), ACADVL (very long-chain acyl-CoA dehydrogenase), and HADHA (hydroxyacyl-CoA dehydrogenase trifunctional multienzyme complex subunit alpha) for ??-oxidation, or to DGAT (diacylglycerol acyltransferase) and GPAT (glycerol-3-phosphate acyltransferase) for lipid storage. Consequently, ACSL1 disruption impairs the formation of lipid droplets and alters the cellular pool of acyl-CoA, influencing processes such as ferroptosis susceptibility and insulin sensitivity.
In Jurkat T cells, ACSL1 knockout is expected to dysregulate fatty acid handling, potentially reducing the supply of acetyl-CoA from ??-oxidation and diminishing ATP generation, which can impair the metabolic flexibility required for rapid proliferation and TCR signaling. Given that Jurkat cells rely on both glycolysis and oxidative metabolism, loss of ACSL1 may shift the lipidome, affecting membrane phospholipid composition and raft dynamics that are critical for receptor clustering and signal transduction. This model thus provides a tool to dissect how lipid metabolism supports leukemic T cell growth and survival, and how it interfaces with pathways such as PPAR signaling and ferroptotic cell death.
This polyclonal knockout product is suited for a range of advanced investigations, including lipidomic profiling, metabolic flux analysis using Seahorse technology, ferroptosis induction with erastin, and functional assays for T cell activation (e.g., CD69 and CD25 flow cytometry). It can also serve as a platform for genetic or pharmacological rescue experiments and for screening compounds that target metabolic vulnerabilities in T cell leukemia. For additional information or custom formats, please contact Ascent Research.
