The ARSA Knockout Jurkat Polyclonal Cells represent a CRISPR/Cas9-mediated polyclonal knockout cell population generated from the Jurkat T-acute lymphoblastic leukemia cell line. This product is a mixed population of cells carrying a range of independent genomic disruptions specifically targeting the ARSA gene, which encodes the lysosomal enzyme arylsulfatase A. The polyclonal format preserves genetic heterogeneity while ensuring near-complete loss of ARSA function at the population level, making it suitable for robust loss-of-function studies. Unlike monoclonal derivatives, these cells avoid the confounding effects of clonal drift and adaptation, providing a more physiologically relevant model for investigating ARSA-dependent processes.
Jurkat cells are an immortalized human T-lymphocyte line originally established from the peripheral blood of a 14-year-old male with acute T-cell leukemia. They grow in suspension and are widely used as a model for T-cell receptor (TCR) signaling and leukemogenesis. The Jurkat host exhibits active lysosomal and sphingolipid metabolic pathways, making it an appropriate cellular context for studying lysosomal storage disorders such as metachromatic leukodystrophy. This suspension culture system allows for scalable experiments and is compatible with standard cell-based assays including flow cytometry, immunofluorescence, and biochemical analyses.
Arylsulfatase A (ARSA) is a lysosomal hydrolase that catalyzes the desulfation of cerebroside sulfate (sulfatide) to cerebroside, a critical step in myelin catabolism and sphingolipid degradation. Its expression and activity are regulated upstream by transcription factor EB (TFEB), a master regulator of lysosomal biogenesis, and nutrient-sensing pathways. ARSA functions in concert with its activator protein Saposin B, which presents sulfatide substrates for enzymatic cleavage. Loss of ARSA activity in this knockout model leads to accumulation of sulfatide within lysosomes, disrupting the lysosomal sphingolipid degradation pathway and downstream processes including cerebroside generation and sulfatide clearance.
In the Jurkat T-cell background, ARSA deficiency provides a unique platform to investigate how sulfatide accumulation affects lymphocyte physiology, including lysosomal function, receptor signaling, and cellular homeostasis. The Jurkat line’s robust growth and well-characterized signaling networks facilitate high-throughput interrogation of ARSA-related pathways and their interplay with T-cell biology. Researchers can use these cells to dissect the impact of lysosomal dysfunction on immune cell viability, proliferation, and signal transduction, offering insights into the systemic manifestations of lysosomal storage disorders.
These ARSA KO Jurkat cells are ideally suited for a range of applications, including modeling metachromatic leukodystrophy pathology, studying sulfatide accumulation dynamics via mass spectrometry, and screening small-molecule correctors or enzyme replacement therapies. They support functional assays such as Western blotting and RT-qPCR to confirm ARSA disruption, LysoTracker staining for lysosomal expansion, immunofluorescence for lysosomal markers, and biochemical enzyme activity measurements. Furthermore, the cells can be employed in drug discovery pipelines targeting lysosomal biogenesis modulators. For additional technical details or custom services, please contact Ascent Research.
