FRRS1 Double Nickase Plasmid (h): sc-406348-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- FRRS1 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
- FRRS1 Double Nickase Plasmid (h) and FRRS1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting FRRS1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
FRRS1 Double Nickase Plasmid (h) | sc-406348-NIC | 20 µg | $410.00 | |||
FRRS1 Double Nickase Plasmid (h2) | sc-406348-NIC-2 | 20 µg | $410.00 |
FRRS1 (ferric chelate reductase 1) encodes a membrane-associated protein implicated in cellular redox biology and iron handling, supporting the reduction of ferric iron and influencing intracellular metal homeostasis. Through effects on iron availability and oxidative balance, FRRS1 can modulate metabolic state and stress responses that intersect with pathways controlling mitochondrial function and reactive oxygen species. Altered iron/redox regulation is broadly relevant to neurobiology and other high-energy tissues, where dysregulated metal homeostasis can contribute to cellular vulnerability. FRRS1 is therefore studied in the context of mechanisms linking iron metabolism to proteostasis, neuronal signaling integrity, and disease-associated stress phenotypes.
FRRS1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the FRRS1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within FRRS1. 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 FRRS1 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 FRRS1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.