Date published: 2026-7-11

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LRIG1 Double Nickase Plasmid (h): sc-403210-NIC

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • LRIG1 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
  • LRIG1 Double Nickase Plasmid (h) and LRIG1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting LRIG1. One or both designs may be available
  • Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: LRIG1 Antibody (B-2): sc-514577
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    LRIG1 Double Nickase Plasmid (h)

    sc-403210-NIC
    20 µg
    $410.00

    LRIG1 Double Nickase Plasmid (h2)

    sc-403210-NIC-2
    20 µg
    $410.00

    LRIG1 encodes a transmembrane leucine-rich repeat and immunoglobulin-like domain protein that acts as a negative regulator of receptor tyrosine kinase signaling. By promoting attenuation and turnover of EGFR/ERBB family receptors and modulating downstream MAPK/ERK and PI3K/AKT pathways, LRIG1 helps control epithelial proliferation, differentiation, and tissue homeostasis. Altered LRIG1 expression or function has been linked to dysregulated growth factor signaling in multiple tumor contexts and to changes in stem or progenitor cell behavior. LRIG1 is therefore widely studied in mechanisms of signal dampening, feedback control, and receptor trafficking.

    LRIG1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the LRIG1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within LRIG1. 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 LRIG1 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 LRIG1-disrupted clones.

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