The KCNJ2 Knockout 786-O Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the 786-O renal cell carcinoma line. This product provides a heterogeneous pool of cells with disrupted KCNJ2 gene function, generated via CRISPR/Cas9-mediated gene disruption. It is designed for loss-of-function studies of KCNJ2, encoding the inward rectifier potassium channel Kir2.1, in a cancer-relevant context. The polyclonal format eliminates clonal selection, allowing rapid functional analysis of pooled editing outcomes.
The 786-O cell line is a well-characterized model of clear cell renal cell carcinoma (ccRCC), derived from a primary tumor. It carries VHL mutations leading to constitutive HIF activation, relevant for studying hypoxia signaling. 786-O cells exhibit a mesenchymal morphology and robust growth, suitable for diverse in vitro assays. This background is ideal for investigating ion channel roles in renal cancer biology, particularly under hypoxic conditions typical of the tumor microenvironment.
KCNJ2 encodes Kir2.1, a strong inward rectifier potassium channel essential for maintaining resting membrane potential and potassium homeostasis. Kir2.1 is regulated by PIP2, PKA, PKC, and adrenergic signals, and interacts with SAP97, PSD-95, filamin A, and caveolin-3 for proper localization. Its activity couples to phospholipase C and CaMKII pathways, influencing cellular excitability, calcium signaling, and cell volume. Disruption of KCNJ2 is predicted to perturb these networks, altering proliferation, migration, and apoptosis.
In 786-O cells, KCNJ2 knockout facilitates dissection of potassium channel contributions to ccRCC pathophysiology. Aberrant ion channel function impacts cancer hallmarks like proliferation and metastasis. Kir2.1 may influence tumor behavior via membrane potential-dependent calcium entry and volume regulation. This model allows assessment of KCNJ2 loss on viability, migration, and hypoxia sensitivity. The polyclonal population captures editing heterogeneity, reflecting genetic variability in tumors and enabling evaluation of overall functional outcomes.
This polyclonal knockout model is applicable to studies of potassium channel biology in renal cancer, tumor microenvironment interactions, and channelopathy disease modeling (Andersen-Tawil syndrome, long QT syndrome type 7). Representative assays include patch-clamp electrophysiology, membrane potential dye-based assays, western blotting, RT-qPCR, and functional tests for proliferation, migration, and apoptosis. The cells are suited for high-throughput drug screening targeting Kir2.1-dependent processes. For technical inquiries or custom projects, contact Ascent Research.
