DIO2 Double Nickase Plasmid (h): sc-402262-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- DIO2 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
- DIO2 Double Nickase Plasmid (h) and DIO2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting DIO2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
DIO2 Double Nickase Plasmid (h) | sc-402262-NIC | 20 µg | $410.00 | |||
DIO2 Double Nickase Plasmid (h2) | sc-402262-NIC-2 | 20 µg | $410.00 |
Human DIO2 encodes type II iodothyronine deiodinase (DIO2), a selenoenzyme that catalyzes outer-ring deiodination of thyroxine (T4) to generate the active thyroid hormone triiodothyronine (T3). By controlling local intracellular T3 availability, DIO2 shapes thyroid hormone receptor–dependent transcriptional programs that influence energy metabolism, thermogenesis, and differentiation in a tissue- and context-specific manner. DIO2 activity is integrated with pathways governing mitochondrial function, oxidative metabolism, and adaptive responses to environmental cues, including nutrient and temperature signals. Altered DIO2 expression or activity has been associated with metabolic phenotypes and thyroid hormone–related dysregulation, supporting its relevance for mechanistic studies in endocrine and metabolic research.
DIO2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the DIO2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within DIO2. 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 DIO2 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 DIO2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.