MCT3 Double Nickase Plasmid (h): sc-403973-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- MCT3 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
- MCT3 Double Nickase Plasmid (h) and MCT3 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting SLC16A8. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MCT3 Double Nickase Plasmid (h) | sc-403973-NIC | 20 µg | $410.00 | |||
MCT3 Double Nickase Plasmid (h2) | sc-403973-NIC-2 | 20 µg | $410.00 |
SLC16A8 encodes monocarboxylate transporter 3 (MCT3), a proton-linked solute carrier that mediates transmembrane transport of lactate and other monocarboxylates, supporting cellular pH homeostasis and metabolic coupling. In human ocular tissues, MCT3 is enriched in the retinal pigment epithelium and contributes to lactate efflux from the outer retina, linking glycolytic flux to oxidative metabolism across epithelial barriers. As a member of the SLC16 family, MCT3 functions within broader monocarboxylate transport and acid–base regulation pathways that influence redox balance and metabolite signaling. Altered monocarboxylate handling and dysregulated lactate transport have been implicated in retinal physiology and disease-relevant processes, making SLC16A8 a useful target for investigating metabolic transport mechanisms.
MCT3 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the SLC16A8 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within SLC16A8. 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 SLC16A8 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 SLC16A8-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.