The KCNJ2 Knockout T-47D Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population featuring targeted disruption of the KCNJ2 gene in the T-47D human breast cancer cell line. This product delivers a heterogeneous loss-of-function model for studying the inward rectifier potassium channel Kir2.1, enabling population-level analyses that average out clonal artifacts.
T-47D is a well-characterized breast ductal carcinoma epithelial cell line derived from the pleural effusion of an invasive ductal carcinoma. It is estrogen receptor (ER)-positive, progesterone receptor (PR)-positive, and HER2-negative, classifying it as the luminal A molecular subtype. Widely used as a model of hormone-responsive breast adenocarcinoma, T-47D cells are essential for investigating ER signaling and endocrine therapy resistance.
KCNJ2 encodes the Kir2.1 inward rectifier potassium channel, which mediates strong inward rectifier current to set and stabilize the resting membrane potential. Kir2.1 is activated by the lipid PIP2 and regulated by upstream signals including cAMP-PKA, PKC, intracellular pH, and estrogen receptor pathways. It associates with scaffolding proteins SAP97 and CASK, the dystrophin-associated complex through alpha-syntrophin, and caveolin-3 for subcellular localization. Membrane potential control by Kir2.1 governs calcium influx, thereby influencing downstream effectors such as NFAT transcription factor, CREB phosphorylation, and cell cycle regulatory proteins. Consequently, KCNJ2 functions as a pivotal node linking electrical membrane properties to intracellular signaling cascades that control cell growth and survival.
In the T-47D luminal breast cancer context, knockout of KCNJ2 likely causes membrane depolarization, perturbing calcium-dependent signaling that intersects with estrogen-driven proliferative and anti-apoptotic programs. This model therefore provides a unique platform to dissect the contributions of Kir2.1 to breast cancer cell proliferation, apoptosis sensitivity, migration, and potential drug resistance. Elucidating these roles may reveal novel ion channel-based vulnerabilities in ER-positive breast cancers.
Researchers can apply this polyclonal knockout product in electrophysiological characterization using patch clamp, membrane potential measurements with fluorescent dyes, and calcium imaging to monitor signaling dynamics. Functional assays such as MTT for viability, Annexin V for apoptosis, and transwell migration studies enable phenotypic profiling. Transcriptomic analysis by RNA-seq, gene expression quantification by RT-qPCR, and protein validation by Western blotting allow comprehensive pathway interrogation. Typical research applications include drug screening for ion channel modulators, investigation of endocrine therapy resistance, and broader studies of potassium channel roles in cancer biology. For further technical details or custom inquiries, please contact Ascent Research.
