The HEXB Knockout Jurkat Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human Jurkat T lymphocyte line. This model features targeted disruption of the HEXB gene, resulting in loss of beta-hexosaminidase subunit beta function. The polyclonal format provides a heterogeneous pool of cells with gene-editing events at the population level, suitable for studying HEXB-dependent lysosomal processes without clonal isolation.
Jurkat cells are an immortalized human CD4-positive T lymphocyte line originally established from the peripheral blood of an acute T cell leukemia patient. Widely employed in T cell signaling, HIV research, and immunological studies, Jurkat cells offer a robust and well-characterized model system. Their transformed phenotype and active transcriptional machinery facilitate the study of gene function in a T cell context.
HEXB encodes the beta subunit of the lysosomal enzyme beta-hexosaminidase, which heterodimerizes with the alpha subunit (HEXA) to form the HexA enzyme complex. This complex, in concert with the GM2 activator protein (GM2A), catalyzes the removal of N-acetylgalactosamine from GM2 ganglioside, yielding GM1 and further degradation products such as GA2 and ceramide. HEXB expression is transcriptionally regulated by the master lysosomal biogenesis factors TFEB and MITF, positioning beta-hexosaminidase within a broader lysosomal gene network. Disruption of HEXB abrogates HexA activity, leading to lysosomal accumulation of GM2 gangliosides and related glycosphingolipids, which can secondarily impact downstream pathways including autophagy and lipid signaling.
In Jurkat T lymphocytes, HEXB knockout recapitulates key molecular hallmarks of Sandhoff disease and GM2 gangliosidosis, enabling investigation of ganglioside accumulation within an immune cell environment. The concomitant lysosomal dysfunction may perturb T cell receptor signaling, vesicular trafficking, and metabolic homeostasis, offering a platform to explore how lysosomal storage disorders intersect with immune cell physiology. This model is particularly valuable for studying the cell-autonomous effects of glycosphingolipid dysregulation in T cells.
This product supports a spectrum of experimental applications, including mechanistic studies of Sandhoff disease pathology, screening of enzyme replacement therapies or pharmacological chaperones, and assessment of ganglioside accumulation on T cell activation and cytokine production. Researchers can validate HEXB disruption via Western blotting and beta-hexosaminidase enzymatic assays, and monitor lipid buildup using immunofluorescence for GM2 ganglioside, lipidomics, and lysosomal staining. Autophagy flux assays further enable characterization of downstream lysosomal-autophagic crosstalk. For technical inquiries and additional product information, please contact Ascent Research.
