DIO3 Double Nickase Plasmid (m): sc-430733-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- DIO3 Double Nickase Plasmid (m) 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
- DIO3 Double Nickase Plasmid (m) and DIO3 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Dio3. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
DIO3 Double Nickase Plasmid (m) | sc-430733-NIC | 20 µg | $410.00 |
Mouse Dio3 encodes type 3 iodothyronine deiodinase (DIO3), an ER- and plasma membrane–associated selenoenzyme that inactivates thyroid hormones by converting T4 to reverse T3 and T3 to T2, thereby restricting local thyroid hormone signaling. By shaping intracellular T3 availability, DIO3 influences thyroid hormone receptor–dependent transcriptional programs that regulate proliferation, differentiation, metabolism, and developmental timing. Dio3 is an imprinted gene within the Dlk1–Dio3 locus and is prominently involved in fetal tissue patterning and neurodevelopmental processes where tight control of thyroid hormone action is required. Dysregulated DIO3 activity or imprinting at this locus has been linked to altered endocrine homeostasis and has been studied in contexts including developmental abnormalities and tumor biology where thyroid hormone signaling impacts cell state.
DIO3 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Dio3 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Dio3. 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 Dio3 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 Dio3-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.