The ARSB Knockout Jurkat Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Jurkat T lymphocyte line, featuring targeted disruption of the ARSB gene. This loss-of-function model is generated through CRISPR/Cas9-mediated gene disruption to ablate arylsulfatase B expression, enabling investigation of glycosaminoglycan catabolism and lysosomal biology.
Jurkat cells are an immortalized human T lymphocyte line originally derived from a 14-year-old male with acute T cell leukemia. Widely used in immunological research, they serve as a well-established model for T cell receptor signaling, apoptosis, and lymphocytic function. The Jurkat background provides a robust and reproducible host for studying the intersection of lysosomal metabolism and T cell physiology.
The ARSB gene encodes the lysosomal enzyme arylsulfatase B, which catalyzes the hydrolysis of 4-sulfate groups from dermatan sulfate and chondroitin sulfate within the glycosaminoglycan degradation pathway. ARSB activity is essential for the stepwise breakdown of these sulfated polymers, and its function depends on modification by the sulfatase-modifying factor SUMF1. ARSB operates within a network of lysosomal hydrolases including IDUA, IDS, SGSH, NAGLU, GNS, and GALNS. Expression of lysosomal genes is transcriptionally regulated by TFEB, MITF, and TFE3, which are themselves controlled by mTORC1 kinase signaling. Disruption of ARSB leads to lysosomal accumulation of partially degraded glycosaminoglycans, impairing downstream catabolic processes and disrupting lysosomal-autophagic flux.
In the Jurkat T lymphocyte background, ARSB knockout creates a powerful tool for examining how lysosomal dysfunction impacts immune cell homeostasis, autophagic clearance, and cellular stress responses. Because T cells rely on functional lysosomes for antigen presentation, receptor turnover, and metabolic adaptation, the loss of arylsulfatase B provides a disease-relevant model to study lysosomal storage disorder pathology in immune cells. This system allows dissection of mTORC1?CTFEB/TFE3 axis regulation and its consequences on lysosomal biogenesis in a lymphocytic environment.
This polyclonal knockout cell population is suited for applications such as mucopolysaccharidosis type VI disease modeling, analysis of glycosaminoglycan accumulation via DMMB assays, LysoTracker staining for lysosomal mass, and evaluation of autophagic markers like LC3B by immunofluorescence or Western blot. Researchers may employ RT-qPCR or RNA-seq to profile transcriptomic changes resulting from ARSB loss and to test enzyme replacement therapies or small-molecule modulators. For further information about this product, contact Ascent Research.
