GPR172A Double Nickase Plasmid (h): sc-405622-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- GPR172A 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
- GPR172A Double Nickase Plasmid (h) and GPR172A Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting SLC52A2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
GPR172A Double Nickase Plasmid (h) | sc-405622-NIC | 20 µg | $410.00 |
SLC52A2 encodes GPR172A, a human riboflavin (vitamin B2) transporter that mediates cellular uptake of riboflavin required for synthesis of FMN and FAD cofactors. By supporting flavoprotein-dependent redox reactions, GPR172A contributes to mitochondrial oxidative metabolism, fatty acid oxidation, and maintenance of cellular redox homeostasis. Perturbation of riboflavin transport impacts energy production and can alter vulnerability to oxidative stress, linking SLC52A2 dysfunction to neurodevelopmental and neuromuscular phenotypes reported in riboflavin transporter deficiency. This gene is therefore relevant for studies of nutrient transport, metabolic regulation, and mitochondrial stress responses in human cell models.
GPR172A Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the SLC52A2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within SLC52A2. 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 SLC52A2 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 SLC52A2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.