TGF beta Receptor 2/TGFBR2 Double Nickase Plasmid (h): sc-400144-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TGF beta Receptor 2/TGFBR2 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
- TGF beta Receptor 2/TGFBR2 Double Nickase Plasmid (h) and TGF beta Receptor 2/TGFBR2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting TGFBR2. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: TGF beta Receptor 2/TGFBR2 Antibody (C-4): sc-17791
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TGF beta Receptor 2/TGFBR2 Double Nickase Plasmid (h) | sc-400144-NIC | 20 µg | $410.00 | |||
TGF beta Receptor 2/TGFBR2 Double Nickase Plasmid (h2) | sc-400144-NIC-2 | 20 µg | $410.00 |
TGFBR2 encodes transforming growth factor beta receptor 2 (TGF-βR2), a transmembrane serine/threonine kinase that binds TGF-β ligands and initiates canonical SMAD2/3 signaling via phosphorylation of TGFBR1, as well as crosstalk with MAPK, PI3K/AKT, and Rho-family pathways. Through these networks, TGF-βR2 regulates epithelial–mesenchymal transition, cell-cycle control, immune modulation, and extracellular matrix homeostasis, shaping tissue development and wound repair. Altered TGFBR2 function or expression perturbs pathway fidelity and is associated with dysregulated fibrosis programs and oncogenic processes, including changes in growth inhibition, invasion, and tumor microenvironment signaling. Because TGF-β signaling is highly context dependent, TGFBR2 is frequently studied to dissect cell-type-specific transcriptional responses and feedback control within cytokine and stress-response circuits.
TGF beta Receptor 2/TGFBR2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the TGFBR2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within TGFBR2. 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 TGFBR2 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 TGFBR2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.