NaDC-1 Double Nickase Plasmid (m): sc-422975-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- NaDC-1 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
- NaDC-1 Double Nickase Plasmid (m) and NaDC-1 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Slc13a2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
NaDC-1 Double Nickase Plasmid (m) | sc-422975-NIC | 20 µg | $410.00 |
Slc13a2 encodes the sodium-dependent dicarboxylate cotransporter NaDC-1, an apical membrane transporter that couples the Na+ gradient to uptake of Krebs cycle intermediates such as citrate, succinate, and α-ketoglutarate. In mouse kidney proximal tubule, NaDC-1 contributes to citrate reabsorption and thereby influences urinary citrate levels, acid–base homeostasis, and calcium salt handling. By regulating intracellular dicarboxylate availability, NaDC-1 can affect mitochondrial anaplerosis and metabolic network flux connected to the TCA cycle. Altered Slc13a2/NaDC-1 function has been linked to kidney stone–relevant phenotypes, renal tubular transport physiology, and metabolic adaptations studied in nephrology and systems metabolism models.
NaDC-1 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Slc13a2 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Slc13a2. 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 Slc13a2 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 Slc13a2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.