C20orf54 Double Nickase Plasmid (h): sc-405094-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- C20orf54 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
- C20orf54 Double Nickase Plasmid (h) and C20orf54 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting SLC52A3. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
C20orf54 Double Nickase Plasmid (h) | sc-405094-NIC | 20 µg | $410.00 | |||
C20orf54 Double Nickase Plasmid (h2) | sc-405094-NIC-2 | 20 µg | $410.00 |
SLC52A3, also known as C20orf54, encodes a high-affinity riboflavin transporter that mediates cellular uptake of vitamin B2, a precursor for FMN and FAD required for flavoprotein-dependent redox reactions. By sustaining flavin cofactor availability, C20orf54 supports mitochondrial oxidative metabolism, fatty acid β-oxidation, and broader cellular redox homeostasis. Altered SLC52A3 activity has been associated with riboflavin transporter deficiency phenotypes and neurodevelopmental and neuromuscular dysfunction linked to impaired flavin-dependent pathways. In cancer biology, SLC52A3 expression has been explored as a metabolic determinant influencing cofactor supply and oxidative stress responses.
C20orf54 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the SLC52A3 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within SLC52A3. 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 SLC52A3 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 SLC52A3-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.