The KCNJ2 Knockout MCF-7 Polyclonal Cells represent a CRISPR/Cas9-mediated gene-disrupted polyclonal cell population derived from the MCF-7 human breast adenocarcinoma cell line. This product provides a loss-of-function model for KCNJ2, the gene encoding the inward rectifier potassium channel Kir2.1. The polyclonal composition ensures representation of multiple editing events within the population, enabling robust functional studies without isolation of single-cell clones. This knockout model is suitable for investigations into potassium channel biology in breast cancer cells.
The host cell line, MCF-7, is an estrogen receptor-positive epithelial cell line originally isolated from a human breast adenocarcinoma. MCF-7 cells are widely employed as a model system for hormone-responsive breast cancer and retain epithelial characteristics, including expression of estrogen receptors and responsiveness to steroid hormones. This well-characterized line serves as a foundational platform for exploring the intersection of ion channel function and oncogenic signaling.
KCNJ2 encodes Kir2.1, which mediates potassium influx at hyperpolarized membrane potentials, thereby stabilizing the resting membrane potential and regulating cellular excitability. Kir2.1 activity is tightly controlled by phosphatidylinositol 4,5-bisphosphate (PIP2) binding and phosphorylation by protein kinase A (PKA) and protein kinase C (PKC), and is modulated by G?¦? subunits, Mg2?, and polyamines such as spermine. The channel interacts with scaffolding proteins including PSD-95, CASK, SAP97, filamin A, syntrophin, and the dystrophin complex, linking it to cytoskeletal and signaling networks. Downstream, Kir2.1-mediated potassium flux influences membrane potential, voltage-gated calcium channel activity, and intracellular calcium signaling, placing it at a critical node in the regulation of membrane potential-dependent processes.
In MCF-7 breast cancer cells, disruption of KCNJ2 is predicted to alter resting membrane potential and perturb potassium homeostasis, with consequences for calcium dynamics, cellular proliferation, apoptosis, and migration. Given the emerging roles of ion channels in cancer progression, this knockout model enables dissection of Kir2.1 contributions to estrogen receptor-positive breast adenocarcinoma pathophysiology. The polyclonal population facilitates studies of heterogeneous editing outcomes and their collective impact on cellular phenotypes, providing a relevant tool for cancer biology research.
This product is suitable for a range of research applications, including investigation of potassium channel function in breast cancer, drug screening for Kir2.1 modulators, and electrophysiological characterization using patch clamp assays. Researchers can assess KCNJ2 knockout validation via western blotting for Kir2.1 protein or RT-qPCR for mRNA levels. Functional studies may employ fluorescent membrane potential dyes, calcium imaging, and proliferation, apoptosis, or migration assays to evaluate phenotypic changes. Additionally, this model supports mechanistic studies of Andersen-Tawil syndrome and related cardiac arrhythmias by leveraging the MCF-7 background for heterologous expression or comparative analyses. For additional information, please contact Ascent Research.
