FOXD2 Double Nickase Plasmid (h): sc-410785-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- FOXD2 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
- FOXD2 Double Nickase Plasmid (h) and FOXD2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting FOXD2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
FOXD2 Double Nickase Plasmid (h) | sc-410785-NIC | 20 µg | $410.00 | |||
FOXD2 Double Nickase Plasmid (h2) | sc-410785-NIC-2 | 20 µg | $410.00 |
FOXD2 encodes a forkhead box (FOX) family transcription factor that binds DNA through a conserved forkhead/winged-helix domain to regulate cell type–specific gene expression programs. FOXD2 is implicated in developmental and differentiation-associated transcriptional networks, coordinating lineage decisions and maintenance of cellular identity through modulation of promoter and enhancer activity. As a transcriptional regulator, altered FOXD2 activity can perturb downstream pathways controlling proliferation, apoptosis, and morphogenesis, making it relevant to studies of dysregulated gene expression in disease contexts. Its nuclear function and regulatory reach across multiple target loci support investigation of FOXD2-dependent gene networks, chromatin state transitions, and context-specific transcriptional control.
FOXD2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the FOXD2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within FOXD2. 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 FOXD2 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 FOXD2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.