The HELZ2 Knockout HEK293T Polyclonal Cells represent a CRISPR/Cas9-mediated gene-disrupted polyclonal cell population derived from HEK293T human embryonic kidney cells. The knockout ablates HELZ2 expression, providing a loss-of-function system to dissect the transcriptional coactivator functions of this helicase in metabolic signaling. As a polyclonal mixture, the product avoids clonal artifacts while offering a robust model for functional studies of PPAR-associated pathways.
HEK293T cells are immortalized human embryonic kidney epithelial cells transformed by SV40 large T-antigen, derived from the HEK293 line. They are widely employed for transient transfection, protein expression, and virus packaging due to their high transfection efficiency and robust growth. The line retains functional PPAR signaling machinery, making it a relevant host for studying HELZ2-mediated coactivation of peroxisome proliferator-activated receptors.
HELZ2 acts as a ligand-inducible coactivator for PPAR-alpha and PPAR-gamma. Following activation by fatty acids (PPAR-alpha) or thiazolidinediones (PPAR-gamma), these nuclear receptors form heterodimers with RXR and bind PPREs in target gene promoters. HELZ2 is recruited to the complex, interacting with PPAR-alpha, PPAR-gamma, and MED1, and uses its helicase domain to facilitate chromatin remodeling or RNA unwinding, enhancing transcription of lipid?catabolic genes including CPT1A, ACOX1, and UCP2. This promotes fatty acid ??-oxidation and improves insulin sensitivity, linking HELZ2 to metabolic homeostasis.
Disruption of HELZ2 in HEK293T cells eliminates endogenous coactivation of PPAR?dependent transcription, creating a null background for studying metabolic regulation. This model is pertinent to research on metabolic syndrome, obesity, non?alcoholic fatty liver disease, and type 2 diabetes, where impaired lipid handling and insulin resistance are key. The knockout allows unambiguous assignment of HELZ2’s role in PPAR-driven metabolic programs and pharmacological responses.
Researchers can employ these cells in dual-luciferase reporter assays to quantify PPAR transcriptional activity, RT?qPCR and western blotting to assess target gene and protein expression, co?immunoprecipitation to map HELZ2?CPPAR interactions, and fatty acid oxidation flux assays to measure metabolic outputs. The polyclonal knockout population is also suited for high?throughput screening of PPAR modulators and for producing virions to transduce other cell models. For further technical support or custom requests, please contact Ascent Research.
