FGF-3 Double Nickase Plasmid (h): sc-404553-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- FGF-3 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
- FGF-3 Double Nickase Plasmid (h) and FGF-3 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting FGF3. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: FGF-3 Antibody (MSD 1): sc-135
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
FGF-3 Double Nickase Plasmid (h) | sc-404553-NIC | 20 µg | $410.00 | |||
FGF-3 Double Nickase Plasmid (h2) | sc-404553-NIC-2 | 20 µg | $410.00 |
FGF3 encodes fibroblast growth factor 3 (FGF-3), a secreted mitogen that signals primarily through FGFR family receptor tyrosine kinases to regulate embryonic patterning, epithelial–mesenchymal interactions, and tissue morphogenesis. Downstream activity engages canonical RTK pathways, including RAS–MAPK, PI3K–AKT, and PLCγ signaling, influencing proliferation, migration, and differentiation in a context-dependent manner. Dysregulated FGF3 expression or locus alterations have been associated with abnormal developmental programs and oncogenic signaling in select tumor types where FGFR pathway activity is perturbed. As a result, FGF3 is frequently studied in models of growth factor–driven cell fate control, receptor–ligand specificity, and pathway cross-talk.
FGF-3 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the FGF3 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within FGF3. 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 FGF3 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 FGF3-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.