The JAZF1 Knockout HEK293T Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population designed for functional studies of the JAZF1 gene. This product comprises a heterogeneous pool of HEK293T cells with targeted disruption of the JAZF1 locus, achieved through CRISPR/Cas9-mediated gene editing. As a polyclonal knockout, it provides a rapid and accessible loss-of-function model for investigating JAZF1-dependent biological processes without requiring single-cell cloning. The knockout relieves JAZF1-mediated transcriptional repression, enabling direct analysis of downstream gene expression changes and cellular phenotypes.
The host cell line, HEK293T, is a well-established human embryonic kidney epithelial line derived from the HEK293 background. These cells are immortalized via stable integration of adenovirus 5 DNA and express the SV40 large T antigen, which facilitates episomal replication of plasmids containing the SV40 origin of replication. This feature makes HEK293T cells exceptionally efficient for transfection, protein overexpression, and viral production, establishing them as a standard platform for studying signaling pathways, protein interactions, and gene regulation in mammalian cells.
JAZF1 encodes a transcriptional corepressor that interacts with nuclear receptors such as peroxisome proliferator-activated receptor gamma (PPAR??) to modulate gene expression programs involved in metabolism and cell proliferation. As part of a corepressor complex that includes nuclear receptor corepressor (NCoR) and histone deacetylases (HDACs), JAZF1 represses transcription of PPAR?? target genes like lipoprotein lipase (LPL) and fatty acid-binding protein 4 (FABP4). The gene is regulated by metabolic signals including insulin and glucose, and it operates within pathways governing adipogenesis, insulin signaling, and thyroid hormone action. JAZF1 also represses cell cycle regulators such as CCND1 (cyclin D1) while promoting expression of the cyclin-dependent kinase inhibitor CDKN1A (p21), thereby linking metabolic control to proliferative potential.
In the HEK293T context, knockout of JAZF1 disrupts its corepressor activity, resulting in derepression of PPAR??-driven transcriptional programs and potential dysregulation of cell cycle machinery. This model is particularly suitable for dissecting JAZF1 function because HEK293T cells support robust expression of exogenous nuclear receptors and reporters, allowing precise interrogation of JAZF1-dependent repression. The loss-of-function approach can reveal JAZF1’s role in modulating insulin-responsive pathways and its potential tumor suppressor activity, with relevance to type 2 diabetes, obesity, and endometrial stromal sarcoma where JAZF1 is implicated through genetic studies.
Researchers can employ these polyclonal knockout cells in a wide array of applications, including mechanistic studies of metabolic gene regulation, drug target validation for metabolic disorders, and cancer biology investigations focused on JAZF1 alterations in sarcoma. Typical assays include Western blotting to confirm JAZF1 loss, RT-qPCR to measure derepression of PPAR?? targets (e.g., FABP4) and cyclin D1, RNA-sequencing for transcriptome-wide analysis, glucose uptake and lipid accumulation assays for metabolic phenotyping, cell proliferation assays, and co-immunoprecipitation to study JAZF1-nuclear receptor interactions. For further technical information, please contact Ascent Research.
