The HSD17B11 Knockout Jurkat Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Jurkat human T-lymphocyte cell line. This product provides a heterogeneous pool of cells carrying targeted disruptions in the HSD17B11 gene, enabling loss-of-function studies in a leukemia-relevant context without single-cell cloning. The polyclonal format allows researchers to interrogate gene function across diverse genetic backgrounds within a defined cellular model, offering a robust system for steroid metabolism, lipid droplet biology, and oncogenic signaling investigations. By leveraging CRISPR/Cas9-mediated gene disruption, this model circumvents issues of clonal variability and provides a physiologically relevant population for functional genomic screens and pathway analysis.
The Jurkat host cell line is a widely used T-cell leukemia model originally derived from a 14-year-old male with acute T-cell leukemia. These cells are PTEN-deficient, resulting in constitutive activation of the PI3K/AKT signaling axis, which drives proliferation and survival. Jurkat cells serve as a foundational model for studying T-cell receptor (TCR) signaling, apoptosis mechanisms, HIV infection dynamics, and leukemia biology. Their transformed nature and well-characterized signaling networks make them particularly suitable for probing how lipid and steroid metabolic pathways intersect with oncogenic processes.
HSD17B11 encodes a NAD-dependent oxidoreductase that catalyzes the conversion of 17-beta-hydroxysteroids, such as estradiol and testosterone, to their corresponding 17-ketosteroids, estrone and androstenedione, thereby modulating local androgen and estrogen levels. Beyond steroid metabolism, HSD17B11 participates in peroxisomal very long-chain fatty acid elongation by hydrating fatty acyl-CoA intermediates, interacting with ELOVL1-7 elongases and peroxisomal acyl-CoA oxidases. The enzyme also promotes lipid droplet formation and homeostasis, a function closely linked to retinoid metabolism and all-trans retinoic acid levels. Transcription of HSD17B11 is regulated by nuclear receptors including the androgen receptor, estrogen receptor alpha, PPAR??, and the lipogenic factor SREBP1c. It functionally interacts with other hydroxysteroid dehydrogenases such as HSD17B4, HSD3B1, and AKR1C3, as well as peroxisomal protein complexes, positioning it at the crossroads of steroid hormone biosynthesis, fatty acid elongation, and lipid droplet regulation.
In the context of Jurkat T-cell leukemia, loss of HSD17B11 is expected to perturb the delicate balance of endogenous steroid hormone metabolism and lipid stores, potentially impacting membrane composition, signaling microdomain assembly, and energy homeostasis. Given the constitutive PI3K/AKT activation in these cells, HSD17B11 knockout may further alter metabolic reprogramming, contributing to altered proliferation, apoptotic sensitivity, or drug resistance. This model provides a unique platform to study how androgen and estrogen signaling, often considered largely endocrine, can operate in an autocrine/paracrine fashion within lymphocytes, influencing tumor cell fitness and immune evasion.
Researchers can employ this polyclonal knockout population in a variety of assay formats, including Western blotting and RT-qPCR for expression validation, LC-MS-based steroid profiling for quantitative hormone analysis, and BODIPY staining coupled with flow cytometry to assess lipid droplet accumulation. Functional studies may involve MTT proliferation assays, apoptosis detection via annexin V staining, and fatty acid elongation assays using deuterated substrates to trace pathway flux. This model is particularly valuable for investigating the role of steroid metabolism in non-alcoholic fatty liver disease, prostate cancer, androgenetic alopecia, and neurological disorders where HSD17B11-associated pathways are implicated. For additional information or technical support, please contact Ascent Research.
