ZIP10 Double Nickase Plasmid (m): sc-432673-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ZIP10 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
- ZIP10 Double Nickase Plasmid (m) and ZIP10 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Slc39a10. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ZIP10 Double Nickase Plasmid (m) | sc-432673-NIC | 20 µg | $410.00 | |||
ZIP10 Double Nickase Plasmid (m2) | sc-432673-NIC-2 | 20 µg | $410.00 |
Slc39a10 encodes the mouse ZIP10 (SLC39 family) zinc influx transporter that regulates cytosolic Zn²⁺ availability and downstream zinc-dependent enzymatic and transcriptional programs. By controlling zinc entry at cellular membranes, ZIP10 influences processes such as signal transduction, oxidative stress responses, and immune cell function, where zinc acts as a second messenger and cofactor. Altered zinc transport homeostasis has been associated with dysregulated inflammation and metabolic stress, and ZIP10-dependent zinc handling is frequently studied in the context of hematopoietic and epithelial biology. As a result, Slc39a10 is relevant for mechanistic investigations of zinc-regulated pathways including cytokine signaling, redox control, and cellular differentiation programs.
ZIP10 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Slc39a10 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Slc39a10. 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 Slc39a10 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 Slc39a10-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.