ZIP14 Double Nickase Plasmid (h): sc-411756-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ZIP14 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
- ZIP14 Double Nickase Plasmid (h) and ZIP14 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting SLC39A14. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ZIP14 Double Nickase Plasmid (h) | sc-411756-NIC | 20 µg | $410.00 | |||
ZIP14 Double Nickase Plasmid (h2) | sc-411756-NIC-2 | 20 µg | $410.00 |
SLC39A14 encodes the metal ion transporter ZIP14, a plasma membrane and endosomal ZIP family member that mediates cellular uptake of divalent cations, with prominent roles in zinc and manganese homeostasis. ZIP14 activity influences metalloprotein function, oxidative stress responses, and metabolic signaling, and it intersects with inflammatory pathways in hepatocytes and immune cells where cytokine cues can modulate transporter expression. Disrupted ZIP14-dependent metal handling has been linked to altered systemic manganese clearance and neurotoxicity phenotypes, and has also been studied in the context of liver metabolism and inflammatory stress. As a result, SLC39A14 is frequently used to probe metal-dependent regulation of enzyme activity, transporter networks, and stress-adaptation programs in human cell models.
ZIP14 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the SLC39A14 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within SLC39A14. 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 SLC39A14 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 SLC39A14-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.