The KCNJ2 Knockout SK-OV-3 Polyclonal Cells product comprises a population of SK-OV-3 cells that have undergone CRISPR/Cas9-mediated disruption of the KCNJ2 gene, yielding a heterogeneous polyclonal knockout model. This format provides a loss-of-function system for studying inward rectifier potassium channel Kir2.1 without clonal isolation, thereby preserving biological diversity within the edited population. The cells are suitable for experiments requiring bulk gene disruption effects in an ovarian cancer background.
The parental SK-OV-3 cell line is a well-characterized human ovarian adenocarcinoma epithelial model, originally isolated from the ascitic fluid of a patient. These cells exhibit epithelial morphology and are widely employed to investigate ovarian cancer biology, including tumorigenesis, metastasis, and drug sensitivity. Their robust growth characteristics and genetic profile make them a reliable platform for gene-editing applications, enabling direct assessment of KCNJ2 function in a clinically relevant context.
KCNJ2 encodes the Kir2.1 protein, a strongly inward rectifying potassium channel that critically maintains the resting membrane potential and controls cellular excitability. Kir2.1 activity is modulated by upstream regulators such as phosphatidylinositol 4,5-bisphosphate (PIP2), cAMP-dependent protein kinase A (PKA), protein kinase C (PKC), and cholesterol. It directly influences membrane potential and downstream effectors including voltage-gated calcium channels, MAPK1 (ERK2), and AKT1. Additionally, Kir2.1 interacts with scaffolding proteins like DLG1 (SAP97), CAV3 (caveolin-3), SNTB2 (beta-2 syntrophin), MAGI1, and PSD-95, which localize the channel to specific membrane microdomains. Disruption of KCNJ2 alters potassium homeostasis, thereby perturbing membrane potential-dependent calcium influx and downstream signaling cascades that control proliferation and survival.
In SK-OV-3 ovarian cancer cells, KCNJ2 knockout is expected to depolarize the resting membrane potential, potentially dysregulating calcium-dependent pathways and modulating the MAPK/ERK and PI3K/AKT signaling axes. Given the role of ion channels in cancer cell proliferation and migration, this knockout model offers a tool to dissect how Kir2.1-mediated electrical signals intersect with oncogenic networks. The model also provides a renewable source for investigating the contribution of Kir2.1 to ovarian cancer pathophysiology, including its potential influence on drug resistance and metastatic behavior.
Research applications include electrophysiological profiling via patch-clamp recording, functional analysis of Kir2.1 in tumor cell proliferation via MTT assays, and calcium imaging. The polyclonal population is compatible with immunoblotting, RT-qPCR, immunofluorescence, RNA-seq, and migration assays. This product is suitable for screening compounds targeting potassium channels in oncology and exploring membrane potential modulation in cancer. For further technical information, please contact Ascent Research.
