Fnk Double Nickase Plasmid (h): sc-404710-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Fnk 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
- Fnk Double Nickase Plasmid (h) and Fnk Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting PLK3. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Fnk Double Nickase Plasmid (h) | sc-404710-NIC | 20 µg | $410.00 | |||
Fnk Double Nickase Plasmid (h2) | sc-404710-NIC-2 | 20 µg | $410.00 |
PLK3 encodes the serine/threonine kinase Fnk, a polo-like kinase family member implicated in cellular stress responses and checkpoint signaling. Fnk participates in pathways that coordinate DNA damage sensing, cell cycle progression, and apoptosis, with reported roles in modulating MAPK-related signaling and other phosphorylation-dependent networks. By regulating protein substrates during proliferative and stress conditions, PLK3 contributes to maintaining genome stability and controlled cell fate decisions. Dysregulation of PLK3 expression or activity has been associated with altered proliferation and survival programs relevant to cancer biology and other conditions characterized by defective checkpoint control.
Fnk Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the PLK3 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within PLK3. 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 PLK3 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 PLK3-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.