TRβ Double Nickase Plasmid (h): sc-401467-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TRβ 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
- TRβ Double Nickase Plasmid (h) and TRβ Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting THRB. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: TRβ1 Antibody (J51): sc-737
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TRβ Double Nickase Plasmid (h) | sc-401467-NIC | 20 µg | $410.00 | |||
TRβ Double Nickase Plasmid (h2) | sc-401467-NIC-2 | 20 µg | $410.00 |
THRB encodes thyroid hormone receptor beta (TRβ), a ligand-activated nuclear receptor that binds triiodothyronine (T3) and regulates transcription through thyroid hormone response elements. TRβ coordinates programs controlling cellular metabolism, mitochondrial activity, lipid and cholesterol homeostasis, thermogenesis, and differentiation via crosstalk with RXR heterodimerization and co-regulator recruitment. THRB activity is integrated with endocrine signaling and transcriptional networks that shape tissue-specific developmental and metabolic states. Dysregulation of THRB signaling or receptor function is associated with altered thyroid hormone responsiveness and has been studied in contexts of metabolic imbalance and oncogenic transcriptional reprogramming.
TRβ Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the THRB locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within THRB. 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 THRB 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 THRB-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.