Ferroportin-1 Double Nickase Plasmid (m): sc-424774-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Ferroportin-1 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
- Ferroportin-1 Double Nickase Plasmid (m) and Ferroportin-1 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Slc40a1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Ferroportin-1 Double Nickase Plasmid (m) | sc-424774-NIC | 20 µg | $410.00 |
Slc40a1 encodes ferroportin-1, the principal cellular iron exporter that controls systemic and tissue iron distribution by mediating Fe²⁺ efflux from enterocytes, macrophages, hepatocytes, and placental cells. Ferroportin activity is tightly regulated by the hepcidin–ferroportin axis, in which hepcidin binding triggers ferroportin internalization and degradation, linking iron flux to inflammatory and metabolic cues. Through its impact on iron availability, ferroportin-1 influences erythropoiesis, mitochondrial function, oxidative stress responses, and macrophage iron recycling. Dysregulation of Slc40a1-dependent iron handling is relevant to iron overload and iron-restricted states, and is frequently modeled in studies of anemia of inflammation, liver iron metabolism, infection biology, and neuroinflammation.
Ferroportin-1 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Slc40a1 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Slc40a1. 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 Slc40a1 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 Slc40a1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.