Mitoferrin Double Nickase Plasmid (m): sc-426703-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Mitoferrin 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
- Mitoferrin Double Nickase Plasmid (m) and Mitoferrin Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Slc25a37. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Mitoferrin Double Nickase Plasmid (m) | sc-426703-NIC | 20 µg | $410.00 |
Slc25a37 encodes mitoferrin (SLC25A37), an inner mitochondrial membrane carrier that transports ferrous iron into the mitochondrial matrix to support heme synthesis and iron–sulfur (Fe–S) cluster biogenesis. By controlling mitochondrial iron availability, mitoferrin influences oxidative phosphorylation, redox balance, and mitochondrial quality control, particularly in erythroid differentiation where heme demand is high. Dysregulation of SLC25A37-mediated iron trafficking is linked to mitochondrial iron overload, impaired hemoglobinization, and cellular oxidative stress phenotypes relevant to anemia-like and sideroblastic-like mechanisms in model systems. Mouse Slc25a37 studies therefore intersect with pathways governing mitochondrial metabolism, iron homeostasis, and stress signaling.
Mitoferrin Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Slc25a37 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Slc25a37. 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 Slc25a37 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 Slc25a37-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.