FN3KRP Double Nickase Plasmid (h): sc-413205-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- FN3KRP 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
- FN3KRP Double Nickase Plasmid (h) and FN3KRP Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting FN3KRP. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: FN3KRP Antibody (G-1): sc-376717
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
FN3KRP Double Nickase Plasmid (h) | sc-413205-NIC | 20 µg | $410.00 | |||
FN3KRP Double Nickase Plasmid (h2) | sc-413205-NIC-2 | 20 µg | $410.00 |
FN3KRP (fructosamine-3-kinase–related protein) is a member of the FN3K family implicated in protein deglycation and cellular defenses against non-enzymatic glycation. By modulating the turnover of fructosamine/Amadori adducts on proteins, FN3KRP is linked to proteostasis, redox balance, and metabolic stress responses that are relevant to glucose homeostasis. Altered activity within glycation–deglycation pathways can influence accumulation of advanced glycation end products and downstream signaling associated with oxidative stress and inflammation. As a result, FN3KRP is studied in the context of metabolic dysregulation and glycation-associated cellular phenotypes in human cells.
FN3KRP Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the FN3KRP locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within FN3KRP. 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 FN3KRP 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 FN3KRP-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.