ZIP10 Double Nickase Plasmid (h): sc-406811-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ZIP10 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
- ZIP10 Double Nickase Plasmid (h) and ZIP10 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting SLC39A10. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: ZIP10 Antibody (1F6): sc-517167
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ZIP10 Double Nickase Plasmid (h) | sc-406811-NIC | 20 µg | $410.00 |
SLC39A10 encodes ZIP10, a plasma membrane zinc importer that helps regulate intracellular Zn²⁺ availability required for metalloprotein function, redox balance, and transcriptional control. By shaping zinc-dependent signaling and enzyme activity, ZIP10 contributes to processes such as cell differentiation, immune cell function, and stress responses. Altered zinc transport through ZIP family members has been linked to disrupted proliferation and inflammatory signaling in disease-relevant contexts. Studying ZIP10 supports mechanistic work on metal homeostasis pathways and their downstream effects on cellular metabolism and signaling networks.
ZIP10 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the SLC39A10 locus in human 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.