Gas6 Double Nickase Plasmid (m): sc-420490-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Gas6 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
- Gas6 Double Nickase Plasmid (m) and Gas6 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Gas6. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Gas6 Double Nickase Plasmid (m) | sc-420490-NIC | 20 µg | $410.00 | |||
Gas6 Double Nickase Plasmid (m2) | sc-420490-NIC-2 | 20 µg | $410.00 |
Growth arrest–specific 6 (Gas6) encodes a vitamin K–dependent secreted ligand that binds TAM receptor tyrosine kinases, particularly AXL, MERTK, and TYRO3, to regulate cell survival, proliferation, and migration. Gas6–TAM signaling coordinates efferocytosis and dampens innate immune activation by modulating PI3K–AKT, MAPK/ERK, and NF-κB-associated pathways, shaping macrophage and dendritic cell responses. In mouse tissues, Gas6 contributes to vascular homeostasis, platelet function, and tissue repair by integrating cues from apoptotic cells and extracellular matrix remodeling. Dysregulated Gas6/AXL axis activity is frequently studied in inflammation, fibrosis, and tumor-associated microenvironment biology, where it influences immune suppression, epithelial-to-mesenchymal transition programs, and metastatic phenotypes.
Gas6 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Gas6 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Gas6. 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 Gas6 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 Gas6-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.