NRAMP2 Double Nickase Plasmid (m): sc-421958-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- NRAMP2 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
- NRAMP2 Double Nickase Plasmid (m) and NRAMP2 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Slc11a2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
NRAMP2 Double Nickase Plasmid (m) | sc-421958-NIC | 20 µg | $410.00 |
Slc11a2 encodes NRAMP2 (DMT1), a proton-coupled divalent metal ion transporter that mediates cellular uptake of ferrous iron and other transition metals across endosomal and plasma membranes. In mouse cells, NRAMP2 supports transferrin-dependent iron release from endosomes and contributes to intestinal iron absorption, linking it to iron homeostasis, erythropoiesis, and metabolic regulation. NRAMP2 activity intersects with endocytic trafficking and metal-responsive signaling networks that shape mitochondrial function and oxidative stress responses. Dysregulation of Slc11a2 is associated with iron-loading and anemia phenotypes and is broadly relevant to models of neurodegeneration, inflammation, and host–pathogen interactions where metal availability influences cellular fitness.
NRAMP2 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Slc11a2 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Slc11a2. 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 Slc11a2 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 Slc11a2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.