The GPD1L Knouckout Jurkat Polyclonal Cells product consists of a heterogeneous population of Jurkat T lymphoblastoid cells in which the GPD1L gene has been disrupted through CRISPR/Cas9-mediated genome editing. This polyclonal knockout cell pool enables robust loss-of-function analyses without requiring clonal isolation, providing an experimentally flexible tool for studying GPD1L-dependent processes in a human T cell context. The cells are offered as a ready-to-use knockout model, eliminating the need for time-consuming gene disruption workflows.
The Jurkat cell line, derived from the peripheral blood of a patient with T cell acute lymphoblastic leukemia (ALL), is a widely employed suspension cell model for T lymphocyte signaling, activation, and leukemogenesis. These lymphoblastoid cells harbor characteristic surface markers and signaling components that recapitulate aspects of human T cell biology. Consequently, Jurkat cells serve as a versatile host for genetic manipulation to dissect intracellular pathways relevant to immunology and cancer research. The GPD1L knockout in this background permits examination of the gene??s function specifically in a malignant T cell environment.
GPD1L encodes a glycerol-3-phosphate dehydrogenase that catalyzes the reversible oxidation of glycerol-3-phosphate to dihydroxyacetone phosphate, using NAD+ as an electron acceptor and contributing to the glycerol phosphate shuttle and NAD/NADH redox balance. The enzyme also forms complexes with the cardiac sodium channel SCN5A and the chaperone protein MOG1, modulating SCN5A cell surface trafficking and channel activity. Upstream regulators include PPARGC1A (PGC-1??) and HIF-1??, which integrate metabolic and oxygen-sensing signals. Downstream, GPD1L activity influences glycerol-3-phosphate levels, NADH generation, and lipid metabolism intermediates, thereby linking cellular metabolism to ion channel regulation.
In Jurkat T cells, GPD1L knockout offers a unique opportunity to explore non-canonical roles of this enzyme beyond cardiac tissues. Disrupting GPD1L may alter the NAD+/NADH ratio and glycolytic flux, potentially affecting T cell activation, proliferation, and redox-sensitive signaling pathways. Given the connection of GPD1L to Brugada syndrome and sudden infant death syndrome through SCN5A, the polyclonal knockout model can be used as a surrogate to study gene function in a non-myocyte cell type, providing insights into tissue-specific disease mechanisms. The model also facilitates investigation of glycerol metabolism in leukemic lymphoblasts.
Typical applications include western blotting and RT-qPCR for confirmation of target disruption, paired with functional analyses such as NAD+/NADH assays and glycerol-3-phosphate quantification to assess metabolic consequences. RNA sequencing can reveal transcriptomic changes, while flow cytometry permits evaluation of T cell surface phenotype and activation markers. These polyclonal cells thus support diverse research on redox biology, T cell immunometabolism, and the extramyocardial effects of Brugada syndrome-associated genes. For further information or to request ordering details, please contact Ascent Research.
