Axl Double Nickase Plasmid (m): sc-424005-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Axl 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
- Axl Double Nickase Plasmid (m) and Axl Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Axl. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Axl Double Nickase Plasmid (m) | sc-424005-NIC | 20 µg | $410.00 | |||
Axl Double Nickase Plasmid (m2) | sc-424005-NIC-2 | 20 µg | $410.00 |
Axl encodes a receptor tyrosine kinase of the TAM family that is activated by ligands such as GAS6 to regulate cell survival, proliferation, migration, and efferocytosis. In mouse systems, Axl signaling interfaces with PI3K–AKT, MAPK/ERK, and NF-κB pathways and contributes to modulation of innate immune responses and inflammatory tone. Dysregulated Axl activity has been associated with altered immune homeostasis, tissue remodeling, and oncogenic phenotypes including epithelial–mesenchymal transition and invasive behavior in diverse experimental models. Accordingly, Axl is frequently interrogated in studies of tumor biology, fibrotic responses, vascular biology, and microenvironment-driven signaling.
Axl Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Axl locus in mouse 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.