Smad2 Double Nickase Plasmid (h): sc-400475-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Smad2 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
- Smad2 Double Nickase Plasmid (h) and Smad2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting SMAD2. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: Smad2 Antibody (A-11): sc-393312
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Smad2 Double Nickase Plasmid (h) | sc-400475-NIC | 20 µg | $410.00 | |||
Smad2 Double Nickase Plasmid (h2) | sc-400475-NIC-2 | 20 µg | $410.00 |
Human SMAD2 encodes Smad2, a receptor-regulated SMAD that transduces TGF-β and activin/NODAL signals from type I receptors to the nucleus, where it partners with SMAD4 to modulate transcriptional programs controlling cell cycle regulation, differentiation, extracellular matrix remodeling, and immune signaling. Smad2 activity is shaped by C-terminal phosphorylation, nuclear-cytoplasmic shuttling, and crosstalk with MAPK and PI3K/AKT pathways, integrating context-dependent growth and stress cues. Dysregulated SMAD2 signaling has been implicated in altered epithelial–mesenchymal dynamics, fibrotic remodeling, inflammation-associated transcriptional states, and tumor biology through perturbation of canonical TGF-β pathway outputs. As a central node in TGF-β superfamily signaling, SMAD2 is frequently studied to dissect pathway wiring, transcriptional complex assembly, and downstream gene network responses.
Smad2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the SMAD2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within SMAD2. 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 SMAD2 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 SMAD2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.