RNF43 Double Nickase Plasmid (h): sc-403797-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- RNF43 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
- RNF43 Double Nickase Plasmid (h) and RNF43 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting RNF43. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
RNF43 Double Nickase Plasmid (h) | sc-403797-NIC | 20 µg | $410.00 | |||
RNF43 Double Nickase Plasmid (h2) | sc-403797-NIC-2 | 20 µg | $410.00 |
RNF43 encodes a RING-type E3 ubiquitin ligase that functions as a key negative regulator of WNT/β-catenin signaling by ubiquitinating Frizzled receptors and promoting their endocytosis and turnover. Through this receptor-level control, RNF43 helps tune stem cell maintenance, epithelial homeostasis, and context-dependent proliferation and differentiation programs. Its activity is closely linked to the R-spondin/LGR axis and intersects with ubiquitin–proteasome system dynamics that shape membrane receptor availability. Dysregulation or loss-of-function alterations in RNF43 are frequently studied in relation to aberrant WNT pathway activation in gastrointestinal and pancreatic tumor biology and in models of epithelial transformation.
RNF43 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the RNF43 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within RNF43. 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 RNF43 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 RNF43-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.