AQP10 Double Nickase Plasmid (h): sc-413807-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- AQP10 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
- AQP10 Double Nickase Plasmid (h) and AQP10 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting AQP10. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
AQP10 Double Nickase Plasmid (h) | sc-413807-NIC | 20 µg | $410.00 | |||
AQP10 Double Nickase Plasmid (h2) | sc-413807-NIC-2 | 20 µg | $410.00 |
AQP10 encodes aquaporin-10, an integral membrane channel in the major intrinsic protein family that facilitates transmembrane movement of water and small uncharged solutes, including glycerol, thereby contributing to osmotic balance and cellular energy substrate handling. In epithelial contexts, AQP10 supports regulated permeability at plasma membranes and participates in processes linked to fluid transport, nutrient absorption, and metabolic coupling through glycerol flux. Altered aquaporin expression or mislocalization can perturb barrier function and solute homeostasis, making AQP10 a relevant target for studying epithelial physiology and glycerol-dependent metabolic pathways. Research on AQP10 also informs mechanisms connecting membrane transport dynamics to inflammatory and metabolic phenotypes in tissue-specific models.
AQP10 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the AQP10 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within AQP10. 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 AQP10 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 AQP10-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.