FXYD2 Double Nickase Plasmid (h): sc-404044-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- FXYD2 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
- FXYD2 Double Nickase Plasmid (h) and FXYD2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting FXYD2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
FXYD2 Double Nickase Plasmid (h) | sc-404044-NIC | 20 µg | $410.00 | |||
FXYD2 Double Nickase Plasmid (h2) | sc-404044-NIC-2 | 20 µg | $410.00 |
FXYD2 encodes a small single-pass membrane protein that serves as a tissue-specific regulatory subunit of the Na⁺/K⁺-ATPase, modulating pump kinetics and ion homeostasis. In human kidney and other epithelia, FXYD2 contributes to transepithelial sodium handling and cellular osmotic balance, linking it to broader processes such as membrane potential regulation and electrolyte transport. Altered FXYD2 expression or function has been associated with renal tubular physiology and inherited tubulointerstitial disease phenotypes, and has been explored in contexts of metabolic stress responses. Because Na⁺/K⁺-ATPase activity influences downstream signaling and cellular energetics, FXYD2 is a useful target for studying ion-transport–dependent pathways in epithelial biology.
FXYD2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the FXYD2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within FXYD2. 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 FXYD2 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 FXYD2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.