The HSDL2 Knockout Jurkat Polyclonal Cells are a polyclonal population of Jurkat T lymphoblasts engineered by CRISPR/Cas9-mediated disruption of the HSDL2 gene. This product provides a loss-of-function model to study peroxisomal short-chain dehydrogenase/reductase function and its role in lipid metabolism and oncogenic signaling. The polyclonal format preserves population-level heterogeneity while generating a knockout background suitable for functional genomics and drug-target validation studies.
Jurkat cells are an immortalized human CD4+ T lymphoblastoid cell line originally derived from an acute T cell leukemia patient. This cell line has been extensively utilized as a model system to dissect T cell receptor (TCR) signaling, apoptosis, and activation pathways. The CD4+ T lymphocyte background makes Jurkat cells particularly relevant for exploring the intersection of immune cell function and metabolic reprogramming in leukemia biology.
HSDL2 encodes a peroxisomal enzyme that catalyzes key steps in fatty acid ??-oxidation and steroid hormone metabolism, thereby contributing to lipid homeostasis and energy balance. The encoded protein functions downstream of transcriptional regulators including PPAR??, PPAR??, SREBP1, and PGC-1??, and it interacts with peroxisomal factors such as PEX5, HSD17B4, and SCP2. Its activity influences AMPK phosphorylation and mTORC1 signaling, modulating the expression of cell cycle regulators like Cyclin D1 and c-Myc. Disruption of HSDL2 thus perturbs the peroxisomal metabolism?Clipid signaling axis, with downstream consequences for metabolic and proliferative pathways.
In the context of Jurkat T lymphoblasts, HSDL2 loss disrupts the delicate balance of lipid-derived second messengers and metabolic substrates required for TCR-mediated activation and leukemic cell expansion. Given that malignant T cells often exhibit altered lipid metabolism and dependency on peroxisomal function for sustained growth, this knockout model offers a powerful tool to dissect how HSDL2-driven steroid and fatty acid flux influences cancer cell fitness and immune effector programs. It serves as a platform to evaluate whether targeting peroxisomal metabolism can impair leukemia cell proliferation.
Researchers can employ these HSDL2 knockout polyclonal cells in a wide range of investigations, including cancer metabolism studies, T cell activation and metabolic reprogramming assays, lipid droplet dynamics analysis, and therapeutic target validation. Compatible techniques span from Western blot and RT-qPCR for expression profiling, to functional assays such as etomoxir-sensitive palmitate oxidation, BODIPY lipid droplet staining, MTT proliferation, and Annexin V apoptosis detection. Flow cytometry for CD69 and CD25 upregulation can assess T cell activation, while multi-omics approaches (RNA-seq, LC-MS metabolomics) and phospho-protein analysis (p-AMPK, p-AKT) enable in-depth mechanistic dissection. For further details or technical support, please contact Ascent Research.
