The KCNJ2 Knockout UM-UC-3 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population with targeted disruption of the KCNJ2 gene, encoding the inward rectifier potassium channel Kir2.1. This loss-of-function model is generated in the UM-UC-3 human bladder cancer cell line and provides a genetically defined system for investigating potassium channel-dependent cellular processes without clonal isolation.
UM-UC-3 is an epithelial cell line originally derived from a male patient with transitional cell carcinoma of the bladder. These cells retain characteristics of bladder transitional epithelium and are widely employed as a model for urothelial carcinoma research, including studies on tumor cell proliferation, migration, and drug response. Their established use in cancer biology ensures compatibility with a broad range of standard and high-throughput assays for mechanistic and pharmacological investigations.
KCNJ2 encodes the Kir2.1 channel, a critical mediator of inward rectifier potassium currents that stabilize the resting membrane potential and regulate cellular excitability. Channel activity is modulated by upstream regulators including phosphatidylinositol 4,5-bisphosphate (PIP2), protein kinase A (PKA), protein kinase C (PKC), and G-protein-coupled receptors. Kir2.1 physically interacts with scaffolding components of the dystrophin-associated protein complex, such as syntrophins and the MAGUK family protein SAP97, and functions in close coordination with other inward rectifier subunits, notably KCNJ4 and KCNJ12. Downstream, KCNJ2-dependent potassium flux influences membrane potential dynamics, which in turn gate calcium signaling pathways and impact cell cycle regulators, thereby linking ion homeostasis to proliferative control.
In the context of bladder cancer, KCNJ2 knockout disrupts the finely tuned potassium equilibrium that underpins cellular proliferation and survival. UM-UC-3 cells exhibit altered electrophysiological properties upon Kir2.1 loss, potentially affecting calcium influx and downstream proliferation signals. This model is particularly relevant for dissecting the role of potassium channelopathies in epithelial tumor biology and for exploring KCNJ2 as a therapeutic target in cancers where ion channel remodeling contributes to malignant phenotypes.
This polyclonal knockout cell population is ideally suited for applications in ion channel pharmacology, cancer electrophysiology, and drug screening for cardiac or neoplastic disorders. Researchers can employ patch clamp electrophysiology to assess membrane potential changes, calcium imaging to monitor intracellular signaling, and functional assays such as proliferation, migration, and invasion studies. Complementary molecular techniques, including western blotting, immunofluorescence, and cell cycle analysis, enable comprehensive phenotypic characterization. For further technical details and ordering information, please contact Ascent Research.
