R-Spondin3 Double Nickase Plasmid (m2): sc-428439-NIC-2
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- R-Spondin3 Double Nickase Plasmid (m2) 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
- R-Spondin3 Double Nickase Plasmid (m2) and R-Spondin3 Double Nickase Plasmid (m22) encode distinct paired gRNA designs targeting Rspo3. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
R-Spondin3 Double Nickase Plasmid (m2) | sc-428439-NIC-2 | 20 µg | $410.00 |
Mouse Rspo3 encodes R‑Spondin3, a secreted matricellular ligand that potentiates canonical WNT/β‑catenin signaling by engaging LGR receptors and neutralizing the ZNRF3/RNF43 ubiquitin ligase complex to stabilize Frizzled/LRP receptors at the cell surface. It plays central roles in embryonic morphogenesis, vascular development, tissue patterning, and stem/progenitor cell maintenance, integrating with extracellular matrix cues to shape epithelial–mesenchymal and angiogenic programs. Dysregulated RSPO3–WNT axis activity has been implicated in aberrant organogenesis and pathological tissue remodeling, including contexts linked to tumorigenesis and fibrosis. Rspo3 is therefore widely used in mouse models and in vitro systems to interrogate WNT pathway regulation, niche signaling, and developmental gene networks via genome editing, reporter assays, and organoid or endothelial differentiation studies.
R-Spondin3 Double Nickase Plasmid (m2) consists of a matched pair of plasmids engineered for high-specificity editing of the Rspo3 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Rspo3. 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 Rspo3 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 Rspo3-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.