KIR4.1 CRISPR/Cas9 KO Plasmid (m): sc-421231

Overview

Kcnj10 encodes the inwardly rectifying potassium channel KIR4.1, a key regulator of K⁺ buffering and membrane potential in glial and other KIR4.1-expressing cell types in mouse. By controlling extracellular potassium homeostasis and coupling ionic balance to water transport, KIR4.1 supports neuronal excitability, synaptic transmission, and tissue osmoregulation, with functional links to Na⁺/K⁺-ATPase activity and astrocyte-mediated spatial K⁺ redistribution. Perturbation of KIR4.1 function has been associated with abnormal neuroglial signaling, altered seizure susceptibility, and broader neurodevelopmental and neurologic phenotypes, making Kcnj10 a relevant target for mechanistic studies of ion channel biology and glial physiology. In experimental settings, KIR4.1 is also used to interrogate how potassium conductance influences cellular metabolism, network activity, and responses to injury or inflammation.

KIR4.1 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Kcnj10 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Kcnj10 together with the Streptococcus pyogenes Cas9 nuclease. The plasmids also encode GFP, allowing fluorescent identification and enrichment of successfully transfected cells by fluorescence microscopy or flow cytometry.

The multi-guide design increases the likelihood of generating insertions or deletions (indels) that disrupt the Kcnj10 open reading frame following Cas9-mediated double-strand break formation. DNA breaks introduced by the CRISPR/Cas9 system are repaired through endogenous non-homologous end joining (NHEJ) pathways, frequently resulting in frameshift mutations that abolish KIR4.1 protein expression.

This CRISPR knockout system enables efficient generation of Kcnj10-deficient cell models for investigation of KIR4.1 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

Key Features

• sgRNAs targeting Kcnj10 exon(s) critical for KIR4.1 function
• Co-expression of SpCas9 and sgRNA from a single plasmid for simplified delivery
• GFP reporter for identification of transfected cells
• Pool of plasmids targeting multiple Kcnj10 genomic sites to improve knockout efficiency
• Compatible with delivery by transfection

Design Variants

CRISPRs +/- HDRs

• gRNAs encoded by KIR4.1 CRISPR/Cas9 KO Plasmid (m) and KIR4.1 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Kcnj10 locus. One or both targeting designs may be available. See Related Products for availability.
• HDR donor constructs encoded by KIR4.1 HDR Plasmid (m) and KIR4.1 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Kcnj10 homology arms to support homology-directed repair at defined Kcnj10 target sites corresponding to the CRISPR/Cas9 KO designs. HDR donor availability may vary. See Related Products for availability.

For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.