Date published: 2026-7-10

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KIR4.1 Double Nickase Plasmid (h): sc-402244-NIC

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • KIR4.1 Double Nickase Plasmid (h) consists of a pair of plasmids each encoding a D10A mutated Cas9 nuclease and a target-specific 20 nt guide RNA (gRNA) designed to knockout gene expression with greater specificity than its CRISPR/Cas9 KO counterpart
  • Paired gRNA sequences are offset by approximately 20 bp to allow for specific Cas9-mediated double nicking of the genomic DNA, which mimics a DSB
  • One plasmid in the pair contains a puromycin-resistance gene for selection; the other plasmid in the pair contains a GFP marker to visually confirm transfection
  • KIR4.1 Double Nickase Plasmid (h) and KIR4.1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting KCNJ10. One or both designs may be available
  • 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 Double Nickase Plasmid (h)

    sc-402244-NIC
    20 µg
    $410.00

    KIR4.1 Double Nickase Plasmid (h2)

    sc-402244-NIC-2
    20 µg
    $410.00

    KCNJ10 encodes the inwardly rectifying potassium channel subunit KIR4.1, a key determinant of glial and epithelial membrane potential that supports potassium buffering, spatial K+ redistribution, and osmotic homeostasis. In the central nervous system, KIR4.1 activity in astrocytes contributes to extracellular K+ clearance coupled to glutamate uptake and water flux, influencing neuronal excitability and network stability. The channel also participates in ion transport processes in kidney and inner ear epithelia, linking K+ handling to tissue fluid and electrochemical balance. Dysregulation or genetic variation in KCNJ10 has been associated with neurological excitability phenotypes and syndromic channelopathy presentations involving brain, kidney, and auditory function, making it a relevant target for mechanistic studies of ion homeostasis pathways.

    KIR4.1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the KCNJ10 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within KCNJ10. When directed to adjacent sites on opposite DNA strands, the two nickases generate offset single-strand nicks that together produce a staggered double-strand break, requiring coordinated on-target activity from both guides. The resulting DNA break is resolved by endogenous cellular repair pathways, most commonly through non-homologous end joining (NHEJ), leading to insertions or deletions that disrupt KCNJ10 function. By requiring dual sgRNA engagement at the target locus, the double nicking approach enhances editing specificity and provides a complementary CRISPR strategy for applications where additional control over targeting precision is desired.

    To support efficient identification of edited cells, one plasmid encodes GFP for fluorescent visualization of transfected populations, while the companion plasmid carries a puromycin resistance gene for antibiotic selection. Together, these features support efficient enrichment of co-transfected populations and simplify the validation of KCNJ10-disrupted clones.

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