HSDL1 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell population derived from the Jurkat human T lymphocyte cell line, engineered to disrupt the HSDL1 gene locus. This product provides a genetically heterogeneous loss-of-function model, enabling researchers to investigate the consequences of HSDL1 deficiency in a mixed knockout background. The polyclonal format avoids clonal selection artifacts and maintains population-level diversity, facilitating functional studies without the constraints of a single clonal genotype.
The Jurkat cell line is an immortalized human T lymphocyte line originally established from the peripheral blood of a 14-year-old male with acute T cell leukemia. Jurkat cells are widely employed as a model system for studying T cell signaling pathways, apoptosis, and lymphocyte activation. Their robust growth characteristics and well-characterized signaling responses make them an ideal host for gene disruption studies aimed at dissecting molecular mechanisms governing immune cell function and metabolism.
HSDL1 encodes a peroxisomal oxidoreductase belonging to the short-chain dehydrogenase/reductase family, which participates in peroxisomal fatty acid beta-oxidation. This enzyme is regulated by PPAR?? and activated by long-chain fatty acids and fibrates. HSDL1 interacts with peroxins PEX5 and PEX7 for peroxisomal import and utilizes NAD+ and coenzyme A as cofactors. It functions downstream of PPAR?? signaling to catalyze the reduction/oxidation of acyl-CoA intermediates, contributing to the breakdown of very long-chain fatty acids and generation of peroxisomal metabolites. Within the peroxisomal beta-oxidation pathway, HSDL1 acts alongside ACOX1, HSD17B4, SCP2, and ABCD1, linking fatty acid metabolism to lipid homeostasis and cellular energy balance.
In Jurkat T cells, disruption of HSDL1 is expected to impair peroxisomal beta-oxidation, leading to accumulation of very long-chain fatty acids and altered acyl-CoA profiles. This lipid dysregulation may fundamentally alter T cell metabolic reprogramming, membrane composition, and signaling platforms, potentially impacting activation, proliferation, and apoptosis. As T cells rely on metabolic flexibility for effector functions, the HSDL1 knockout model offers a unique tool to examine how peroxisomal lipid metabolism intersects with immune cell functionality and leukemogenesis, given the Jurkat cell??s leukemic origin.
Researchers can apply these polyclonal knockout cells in diverse experimental settings, including Western blotting to confirm HSDL1 protein depletion, RT-qPCR for transcript analysis, immunofluorescence to visualize peroxisome morphology, and fatty acid oxidation assays to measure metabolic fluxes. Additionally, flow cytometry can assess apoptosis and proliferation, while lipidomics and Seahorse metabolic flux analysis provide comprehensive metabolic profiling. ATP assays enable evaluation of cellular energy status. This model is particularly valuable for investigations into peroxisomal disorders, fatty acid oxidation defects, neurodevelopmental disorders, and cancer cell metabolism. For inquiries or technical support, please contact Ascent Research.
