ZIP9 Double Nickase Plasmid (m): sc-435885-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ZIP9 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
- ZIP9 Double Nickase Plasmid (m) and ZIP9 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Slc39a9. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ZIP9 Double Nickase Plasmid (m) | sc-435885-NIC | 20 µg | $410.00 | |||
ZIP9 Double Nickase Plasmid (m2) | sc-435885-NIC-2 | 20 µg | $410.00 |
Slc39a9 encodes ZIP9 (SLC39A9), a member of the ZIP family of metal ion transporters that contributes to cellular zinc homeostasis by regulating zinc influx and compartmental distribution. By shaping intracellular Zn²⁺ availability, ZIP9 influences zinc-dependent enzymes and transcriptional programs, linking metal balance to processes such as membrane trafficking, signaling, and stress responses. Dysregulated zinc transport is broadly associated with altered immune function, metabolic control, and proliferative signaling, making Slc39a9 a useful target for mechanistic studies of metal-dependent pathways. In mouse systems, ZIP9 perturbation supports dissection of zinc-responsive networks and their downstream phenotypes in relevant cell types and tissues.
ZIP9 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Slc39a9 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Slc39a9. 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 Slc39a9 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 Slc39a9-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.