Date published: 2026-7-10

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KIR4.1 CRISPR/Cas9 KO Plasmid (h): sc-402244

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • KIR4.1 CRISPR/Cas9 Knockout (KO) Plasmid (h) is a pool of plasmids, each encoding Cas9 nuclease and a target-specific 20 nt guide RNA (gRNA) designed for maximum knockout efficiency using sequences derived from the GeCKO v2 library
  • gRNA sequences direct Cas9 to induce site-specific double-strand breaks (DSBs) in the KIR4.1 genomic locus, resulting in gene knockout through non-homologous end joining (NHEJ)
  • The puromycin resistance and RFP genes are flanked by LoxP sites, enabling removal of selection markers via Cre recombinase (Cre Vector: sc-418923) after establishing stable knockout cell lines
  • Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: KIR4.1 Antibody (1C11): sc-293252
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    KIR4.1 CRISPR/Cas9 KO Plasmid (h)

    sc-402244
    20 µg
    $397.00

    Overview

    Human KCNJ10 encodes the inwardly rectifying potassium channel KIR4.1, a membrane protein that helps set resting membrane potential and regulates potassium buffering and spatial K+ redistribution in glial and epithelial contexts. KIR4.1 supports ion and water homeostasis through functional coupling to transport processes and contributes to maintenance of extracellular K+ and osmotic balance, influencing neuronal excitability and tissue microenvironment stability. Dysregulated KCNJ10/KIR4.1 activity has been linked to altered glial physiology, disrupted ionic homeostasis, and neurological phenotypes, making it a relevant target for studying ion channel–dependent signaling and homeostatic pathways.

    KIR4.1 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the KCNJ10 gene in human 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 (h) and KIR4.1 CRISPR/Cas9 KO Plasmid (h2) 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 (h) and KIR4.1 HDR Plasmid (h2) 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.