ZNRF2 Double Nickase Plasmid (h): sc-408350-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ZNRF2 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
- ZNRF2 Double Nickase Plasmid (h) and ZNRF2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ZNRF2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ZNRF2 Double Nickase Plasmid (h) | sc-408350-NIC | 20 µg | $410.00 |
Human ZNRF2 encodes a RING-type E3 ubiquitin ligase that contributes to ubiquitin-dependent control of protein turnover and signaling outputs. By modulating substrate ubiquitination, ZNRF2 can influence cellular processes such as receptor and kinase signaling, proteostasis, and pathway adaptation to environmental cues. Dysregulated ubiquitin ligase activity is frequently linked to altered growth control and stress responses, making ZNRF2 a useful node for dissecting mechanisms that connect ubiquitination to pathway rewiring. Research on ZNRF2 supports studies of signaling fidelity, protein stability, and context-dependent regulatory circuits relevant to disease-associated cellular phenotypes.
ZNRF2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ZNRF2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ZNRF2. 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 ZNRF2 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 ZNRF2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.