ZAP Double Nickase Plasmid (m): sc-429710-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ZAP Double Nickase Plasmid (m) 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
- ZAP Double Nickase Plasmid (m) and ZAP Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Zc3hav1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ZAP Double Nickase Plasmid (m) | sc-429710-NIC | 20 µg | $410.00 | |||
ZAP Double Nickase Plasmid (m2) | sc-429710-NIC-2 | 20 µg | $410.00 |
Mouse Zc3hav1 encodes zinc-finger antiviral protein (ZAP), an interferon-stimulated RNA-binding factor that restricts diverse RNA viruses by recognizing CpG-enriched viral transcripts and promoting their degradation. ZAP coordinates antiviral innate immune signaling by engaging RNA decay and translation control pathways and by interfacing with E3 ubiquitin ligase complexes such as TRIM25 to amplify restriction. Through these activities, ZAP helps shape cellular responses to infection and inflammation, influencing interferon-driven transcriptional programs and stress-associated RNA metabolism. Altered ZAP activity has been linked to differences in viral susceptibility and can modulate immune-related phenotypes relevant to infection biology and host–pathogen interactions.
ZAP Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Zc3hav1 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Zc3hav1. 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 Zc3hav1 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 Zc3hav1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.