The KCNJ2 Knockout LoVo Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the LoVo human colorectal adenocarcinoma cell line. This product provides a genetically disrupted KCNJ2 locus, resulting in loss of Kir2.1 inward rectifier potassium channel function, and serves as a controlled model for investigating potassium channel biology in a cancer cell context. The heterogeneous polyclonal population reflects pooled editing outcomes and is suitable for experiments not requiring isogenic clonal selection.
LoVo cells were established from a metastatic supraclavicular lymph node of a male patient with colon adenocarcinoma and are widely used as a model for metastatic colorectal cancer. They harbor an activating KRAS G13D mutation, which drives oncogenic signaling, and exhibit typical epithelial morphology. The LoVo background provides a clinically relevant system to study membrane potential dynamics in a tumor cell line that retains aggressive metastatic characteristics.
KCNJ2 encodes the Kir2.1 inward rectifier potassium channel, which stabilizes the resting membrane potential by mediating potassium efflux. Kir2.1 activity is regulated by phosphatidylinositol 4,5-bisphosphate (PIP2) and is modulated by protein kinase A (PKA) and protein kinase C (PKC) phosphorylation downstream of beta?adrenergic signaling and intracellular magnesium. Channel opening promotes membrane hyperpolarization, which in turn influences voltage?gated calcium channel activity and downstream MAPK/ERK signaling. Kir2.1 interacts with scaffolding proteins DLG1/SAP97 and DLG4/PSD?95, and forms complexes with caveolin?3 (CAV3), syntrophin (SNTA1), and the dystrophin?associated glycoprotein complex, positioning the channel at the intersection of electrical signaling and cytoskeletal organization.
In the LoVo colorectal adenocarcinoma model, loss of Kir2.1 function permits dissection of the channel??s role in cancer cell physiology. Because membrane potential influences proliferation, migration, and apoptosis, this knockout enables study of how Kir2.1?dependent hyperpolarization affects these behaviors in a KRAS G13D?mutant background. Potential crosstalk between Kir2.1 and the MAPK/ERK pathway is particularly relevant, as altered potassium channel activity may impact downstream effectors critical for tumor progression and metastasis.
This polyclonal knockout product supports applications including electrophysiological characterization via patch?clamp recording, screening for small?molecule Kir2.1 modulators, and functional studies linking membrane potential to metastatic behavior. Target gene disruption can be validated by western blotting and immunofluorescence, while proliferation, migration, and apoptosis can be assessed by MTT assay, wound healing, and Annexin V staining, respectively; transcriptomic consequences may be examined by RNA?seq. For further information, please contact Ascent Research.
