Date published: 2026-7-14

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DRAK2 Double Nickase Plasmid (m): sc-430202-NIC

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • DRAK2 Double Nickase Plasmid (m) 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
  • DRAK2 Double Nickase Plasmid (m) and DRAK2 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Stk17b. One or both designs may be available
  • Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: DRAK2 Antibody (C-2): sc-398324
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    DRAK2 Double Nickase Plasmid (m)

    sc-430202-NIC
    20 µg
    $410.00

    Stk17b encodes DRAK2 (DAPK-related apoptosis-inducing kinase 2), a serine/threonine kinase that modulates lymphocyte signaling thresholds and stress-responsive cell fate decisions. In mouse immune cells, DRAK2 has been linked to regulation of T cell receptor–driven calcium signaling and downstream transcriptional programs that influence activation, anergy, and apoptosis. By integrating kinase signaling with mitochondrial and cytoskeletal processes, DRAK2 can affect proliferation and survival in hematopoietic contexts. Dysregulated STK17B/DRAK2 activity has been associated with immune dysfunction and inflammatory disease mechanisms, supporting its use as a node for studying signaling control in immunology and cell death research.

    DRAK2 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Stk17b locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Stk17b. 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 Stk17b 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 Stk17b-disrupted clones.

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