mitochondrial ferritin Double Nickase Plasmid (m): sc-426664-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- mitochondrial ferritin 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
- mitochondrial ferritin Double Nickase Plasmid (m) and mitochondrial ferritin Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Ftmt. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
mitochondrial ferritin Double Nickase Plasmid (m) | sc-426664-NIC | 20 µg | $410.00 |
Mouse Ftmt encodes mitochondrial ferritin, an iron-sequestering protein localized to the mitochondrial matrix that buffers redox-active iron and helps limit reactive oxygen species generation. By storing iron in a ferritin-like shell, Ftmt contributes to mitochondrial iron homeostasis, supports respiratory chain integrity, and influences pathways linked to oxidative stress responses and mitochondrial quality control. Altered mitochondrial iron handling has been connected to neurodegeneration, anemia-related phenotypes, and metabolic stress, making Ftmt a useful locus for studying ferroptosis susceptibility and mitochondrial dysfunction in mammalian cells. Ftmt expression is also leveraged as a readout in models of iron overload and inflammation-associated shifts in cellular iron trafficking.
mitochondrial ferritin Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Ftmt locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Ftmt. 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 Ftmt 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 Ftmt-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.