FOXI1 Double Nickase Plasmid (h): sc-408728-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- FOXI1 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
- FOXI1 Double Nickase Plasmid (h) and FOXI1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting FOXI1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
FOXI1 Double Nickase Plasmid (h) | sc-408728-NIC | 20 µg | $410.00 | |||
FOXI1 Double Nickase Plasmid (h2) | sc-408728-NIC-2 | 20 µg | $410.00 |
FOXI1 (forkhead box I1) is a winged-helix transcription factor that regulates epithelial lineage specification and ion transport programs, particularly in the inner ear and kidney. It modulates transcriptional networks controlling acid–base homeostasis and channel/transport gene expression, integrating with broader developmental and differentiation pathways governed by forkhead family factors. Genetic perturbation of FOXI1 has been linked to syndromic and nonsyndromic disorders involving distal renal tubular function and auditory physiology, making it a useful node for studying epithelial maturation and organ-specific transcriptional control. In cell-based models, FOXI1 activity can be interrogated to connect transcriptional regulation with downstream changes in transporter expression, cellular polarization, and stress-response signaling.
FOXI1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the FOXI1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within FOXI1. 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 FOXI1 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 FOXI1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.