The HMOX2 Knockout HEK293T Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population engineered for targeted disruption of the HMOX2 gene in HEK293T cells. This loss-of-function model uses a heterogeneous pool of edited cells that collectively eliminate heme oxygenase-2 expression, avoiding clonal selection artifacts and offering a population-representative knockout phenotype suitable for studying HMOX2 deficiency in heme catabolism, CO signaling, cytoprotection, and iron homeostasis.
HEK293T is a widely used human embryonic kidney cell line stably expressing SV40 large T antigen, enabling episomal replication of SV40 origin-containing plasmids and high-level protein expression. Its epithelial origin and robust growth support a wide range of biochemical and cell-based assays, including transfection, lentivirus production, and live-cell imaging. Combined with CRISPR/Cas9 knockout, this background provides a powerful, high-throughput-compatible platform for investigating gene function.
HMOX2 encodes heme oxygenase-2, which catalyzes heme cleavage to biliverdin, carbon monoxide (CO), and ferrous iron. Biliverdin is reduced by biliverdin reductase to bilirubin, while CO activates soluble guanylyl cyclase (sGC), elevating cGMP and stimulating PKG. Iron is sequestered by ferritin. HMOX2 is regulated by NRF2, SP1, nitric oxide, and hypoxia, and interacts with NADPH-cytochrome P450 reductase and caveolin-1. Its CO signaling mediates anti-inflammatory and anti-apoptotic effects downstream. Disruption of HMOX2 thereby abolishes this entire cytoprotective and iron-regulatory axis.
In HEK293T cells, HMOX2 knockout removes a major enzymatic source of biliverdin, CO, and the ferritin-bound iron pool, sensitizing cells to oxidative stress and disrupting iron homeostasis. This polyclonal knockout population mimics heterogeneous HMOX2 deficiency, allowing investigation of effects on cell viability, redox balance, and inflammatory signaling without clonal adaptation artifacts. The model further enables study of crosstalk between heme catabolism and pathways like NRF2-driven antioxidant responses and intrinsic apoptosis, supporting therapeutic discovery in neuroprotection and ischemia.
These cells serve for functional validation of HMOX2-targeting drugs, dissection of CO-mediated cytoprotection, and heme?Ciron axis studies. Knockout confirmation uses Western blot, RT-qPCR, and heme oxygenase activity assays. Functional readouts include intracellular iron measurement, ROS detection, and apoptosis assays under oxidative stress. Immunofluorescence and flow cytometry enable spatial and quantitative stress-marker analysis. This polyclonal knockout resource supports academic and pharmaceutical research in neurodegeneration, ischemic injury, and inflammation. For inquiries, contact Ascent Research.
