xCT Double Nickase Plasmid (m): sc-424104-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- xCT 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
- xCT Double Nickase Plasmid (m) and xCT Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Slc7a11. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
xCT Double Nickase Plasmid (m) | sc-424104-NIC | 20 µg | $410.00 |
Slc7a11 encodes xCT, the light chain subunit of the system x_c^- cystine/glutamate antiporter that imports extracellular cystine in exchange for intracellular glutamate. By supplying cystine for glutathione biosynthesis, xCT supports cellular redox buffering and limits lipid peroxidation, linking Slc7a11 to oxidative stress responses and ferroptosis susceptibility. xCT activity intersects with amino acid transport, NRF2-regulated antioxidant programs, and glutamate homeostasis, influencing metabolic adaptation under nutrient limitation. Dysregulated Slc7a11 expression or transport activity has been associated with altered stress tolerance in cancer models, neuroinflammatory contexts, and other conditions where redox imbalance and cell death pathways are key experimental endpoints.
xCT Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Slc7a11 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Slc7a11. 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 Slc7a11 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 Slc7a11-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.