Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
ferritin heavy chain Double Nickase Plasmid (h): sc-418152-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ferritin heavy chain Double Nickase Plasmid (h) 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
- ferritin heavy chain Double Nickase Plasmid (h) and ferritin heavy chain Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting FTH1. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: ferritin heavy chain Antibody (B-12): sc-376594
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ferritin heavy chain Double Nickase Plasmid (h) | sc-418152-NIC | 20 µg | $410.00 | |||
ferritin heavy chain Double Nickase Plasmid (h2) | sc-418152-NIC-2 | 20 µg | $410.00 |
FTH1 encodes the human ferritin heavy chain, a ferroxidase subunit that converts Fe²⁺ to Fe³⁺ to promote safe iron sequestration within ferritin shells and maintain intracellular iron homeostasis. By buffering labile iron and limiting Fenton chemistry, FTH1 influences oxidative stress responses, mitochondrial function, and iron-dependent cell death programs such as ferroptosis. FTH1 expression is regulated by iron-responsive element/iron regulatory protein signaling and intersects with autophagic ferritin turnover (ferritinophagy) via NCOA4 to control iron mobilization. Dysregulated ferritin biology and altered FTH1 levels are frequently linked to inflammation, neurodegeneration, anemia-related states, and tumor-associated metabolic remodeling, making it a useful node for mechanistic studies of iron handling.
ferritin heavy chain Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the FTH1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within FTH1. 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 FTH1 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 FTH1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.