Date published: 2026-9-1

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Axl Double Nickase Plasmid (h): sc-400393-NIC

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • Axl 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
  • Axl Double Nickase Plasmid (h) and Axl Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting AXL. One or both designs may be available
  • Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: Axl Antibody (H-3): sc-166269
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    Axl Double Nickase Plasmid (h)

    sc-400393-NIC
    20 µg
    $410.00

    Axl Double Nickase Plasmid (h2)

    sc-400393-NIC-2
    20 µg
    $410.00

    AXL encodes Axl, a TAM family receptor tyrosine kinase activated by ligands such as GAS6 to regulate cell survival, proliferation, migration, and efferocytosis. Axl signaling engages PI3K–AKT, MAPK/ERK, JAK/STAT, and NF-κB pathways and modulates integrin and cytoskeletal dynamics that influence cell adhesion and motility. In immune and stromal contexts, Axl contributes to resolution of inflammation and phagocytic clearance of apoptotic cells, shaping cytokine signaling and tissue remodeling. Dysregulated AXL expression or activity has been associated with invasive phenotypes and altered immune microenvironments in multiple cancer and inflammatory disease models, supporting mechanistic studies of receptor signaling and pathway cross-talk.

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

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