MCT8 Double Nickase Plasmid (h): sc-403824-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- MCT8 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
- MCT8 Double Nickase Plasmid (h) and MCT8 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting SLC16A2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MCT8 Double Nickase Plasmid (h) | sc-403824-NIC | 20 µg | $410.00 | |||
MCT8 Double Nickase Plasmid (h2) | sc-403824-NIC-2 | 20 µg | $410.00 |
SLC16A2 encodes monocarboxylate transporter 8 (MCT8), a high-affinity and highly specific thyroid hormone transporter that mediates cellular uptake and efflux of triiodothyronine (T3) and thyroxine (T4). By regulating intracellular thyroid hormone availability, MCT8 influences thyroid hormone receptor signaling and downstream transcriptional programs that control neurodevelopment, neuronal differentiation, and metabolic homeostasis. MCT8 activity integrates with membrane transport processes and endocrine signaling to shape tissue-specific thyroid hormone action. Pathogenic variation in SLC16A2 is linked to severe neurodevelopmental phenotypes and altered thyroid hormone distribution, making it a key target for mechanistic studies of thyroid hormone transport and signaling.
MCT8 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the SLC16A2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within SLC16A2. 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 SLC16A2 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 SLC16A2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.