Date published: 2026-7-8

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Artemis Double Nickase Plasmid (h): sc-405295-NIC

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • Artemis 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
  • Artemis Double Nickase Plasmid (h) and Artemis Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting DCLRE1C. One or both designs may be available
  • Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: Artemis Antibody (C-8): sc-518193
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    Artemis Double Nickase Plasmid (h)

    sc-405295-NIC
    20 µg
    $410.00

    DCLRE1C encodes Artemis, a nuclease essential for DNA double-strand break processing during V(D)J recombination and classical non-homologous end joining (c-NHEJ). Artemis functions with the DNA-PK complex to open hairpin coding ends and trim or resolve complex DNA termini, supporting accurate repair and lymphocyte antigen receptor diversification. Disruption of Artemis activity compromises genomic stability and impairs immune cell development, linking DCLRE1C dysfunction to radiosensitivity and severe combined immunodeficiency phenotypes. In research settings, Artemis is commonly studied in the context of DNA damage responses, end-joining pathway choice, and mechanisms governing programmed recombination.

    Artemis Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the DCLRE1C locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within DCLRE1C. 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 DCLRE1C 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 DCLRE1C-disrupted clones.

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