FOXF1 Double Nickase Plasmid (h): sc-403521-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- FOXF1 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
- FOXF1 Double Nickase Plasmid (h) and FOXF1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting FOXF1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
FOXF1 Double Nickase Plasmid (h) | sc-403521-NIC | 20 µg | $410.00 | |||
FOXF1 Double Nickase Plasmid (h2) | sc-403521-NIC-2 | 20 µg | $410.00 |
FOXF1 (Forkhead box F1) encodes a forkhead family transcription factor that regulates mesenchymal differentiation, vascular development, and epithelial–mesenchymal signaling during organogenesis. In human cells, FOXF1 influences transcriptional programs controlling extracellular matrix remodeling, cell migration, and angiogenic gene expression, integrating with developmental signaling networks such as Hedgehog, WNT, and TGF-β/SMAD pathways. Altered FOXF1 dosage or regulatory disruption has been linked to congenital lung and vascular abnormalities and to dysregulated stromal programs in cancer biology. As a lineage and microenvironment regulator, FOXF1 is frequently studied in models of pulmonary mesenchyme, endothelial–stromal interactions, and developmental transcriptional control.
FOXF1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the FOXF1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within FOXF1. 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 FOXF1 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 FOXF1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.