Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Smad2 Double Nickase Plasmid (m): sc-421525-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Smad2 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
- Smad2 Double Nickase Plasmid (m) and Smad2 Double Nickase Plasmid (m2) 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 (YZ-13): sc-101153
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Smad2 Double Nickase Plasmid (m) | sc-421525-NIC | 20 µg | $410.00 | |||
Smad2 Double Nickase Plasmid (m2) | sc-421525-NIC-2 | 20 µg | $410.00 |
Mouse Smad2 encodes an R-SMAD transcription factor that transduces signals from TGF‑β/Activin receptors to the nucleus, where it cooperates with SMAD4 to regulate context-dependent gene expression programs. Through phosphorylation-dependent complex formation and chromatin engagement, SMAD2 controls processes including epithelial–mesenchymal transition, extracellular matrix remodeling, cell-cycle regulation, and lineage specification during development. Smad2 activity intersects with MAPK and PI3K signaling and is modulated by inhibitory SMADs and ubiquitin-mediated turnover, shaping signal duration and amplitude. Dysregulated TGF‑β/SMAD2 signaling is frequently studied in fibrosis, inflammation, and cancer biology, where pathway balance influences proliferation, differentiation, and invasive phenotypes.
Smad2 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Smad2 locus in mouse 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.