The HSD17B11 Knockout HEK293T Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal cell population designed to ablate HSD17B11 function. This heterogeneous pool of edited cells carries targeted disruptions within the HSD17B11 locus, enabling researchers to interrogate the consequences of HSD17B11 loss in a well-characterized human embryonic kidney epithelial cell system. The polyclonal format bypasses the need for clonal isolation and captures a range of editing events, offering a robust model for population-level studies of gene function.
HEK293T cells are a derivative of the HEK293 line, stably expressing the SV40 large T-antigen, which permits episomal replication of plasmids containing the SV40 origin of replication, thereby enhancing transient protein expression and viral production. These cells are valued for their adherent epithelial morphology, high transfectability, and utility in a wide array of applications including recombinant protein expression, lentiviral and retroviral packaging, and biochemical assays. The well-documented growth characteristics and genetic tractability of HEK293T make it an ideal host for generating gene-edited derivatives.
HSD17B11 is a member of the 17??-hydroxysteroid dehydrogenase family, catalyzing the NAD+-dependent oxidation of 17??-hydroxysteroids to their corresponding 17-ketosteroids, thereby modulating steroid hormone levels and participating in lipid and retinoic acid metabolism. Within the steroidogenic network, HSD17B11 activity is transcriptionally regulated by nuclear receptors such as PPARG and LXRA, as well as by androgen receptor signaling, and it functions in concert with related family members HSD17B1, HSD17B2, and HSD17B7, along with AKR1C3 and CYP19A1. Loss of HSD17B11 disrupts the metabolic flux through these pathways, potentially altering the balance of active and inactive steroid hormones and impacting downstream signaling cascades.
In the HEK293T background, disruption of HSD17B11 provides a simplified system to dissect its role in steroid metabolism without the confounding influence of endocrine tissue-specific regulation. Although HEK293T cells are not steroidogenic by nature, their protein expression machinery allows reconstitution of relevant enzyme pathways, making this knockout model valuable for ectopic expression studies of upstream regulators or interacting partners. Furthermore, the high transfectability of HEK293T enables combinatorial experiments??such as co-expression of wild-type or mutant HSD17B11 with PPARG, LXRA, or androgen receptor??to investigate regulatory mechanisms and rescue phenotypes.
This HSD17B11 knockout cell pool is suited for a variety of applications in steroid and lipid metabolism research, including quantitative assessment of steroid hormone profiles by LC-MS/MS, metabolic flux analyses, and drug metabolism assays screening for modulators of 17??-HSD activity. The cells can also be employed in cancer biology studies to explore the potential link between steroid metabolic dysregulation and tumor cell proliferation, and in endocrine function research where altered intracellular hormone levels play a role. Techniques such as RT-qPCR and western blotting allow rapid verification of gene disruption and downstream effects. For further information or to request a quote, please contact Ascent Research.
