GPR172B Double Nickase Plasmid (h): sc-407324-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- GPR172B 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
- GPR172B Double Nickase Plasmid (h) and GPR172B Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting SLC52A1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
GPR172B Double Nickase Plasmid (h) | sc-407324-NIC | 20 µg | $410.00 |
SLC52A1 encodes the human riboflavin transporter RFVT1, also referred to as GPR172B, a membrane protein that mediates cellular uptake of vitamin B2, a precursor for the flavin cofactors FMN and FAD. By controlling intracellular riboflavin availability, GPR172B influences flavoprotein-dependent redox metabolism, mitochondrial energy production, and oxidative stress responses. RFVT1 activity supports biochemical pathways including fatty acid β-oxidation and electron transport that require FAD/FMN-dependent enzymes. Altered riboflavin transport and flavin homeostasis have been associated with metabolic dysfunction and neuromuscular phenotypes linked to impaired vitamin B2 utilization.
GPR172B Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the SLC52A1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within SLC52A1. 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 SLC52A1 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 SLC52A1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.