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.
Smad7 Double Nickase Plasmid (h): sc-400251-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Smad7 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
- Smad7 Double Nickase Plasmid (h) and Smad7 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting SMAD7. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: Smad7 Antibody (B-8): sc-365846
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Smad7 Double Nickase Plasmid (h) | sc-400251-NIC | 20 µg | $410.00 | |||
Smad7 Double Nickase Plasmid (h2) | sc-400251-NIC-2 | 20 µg | $410.00 |
SMAD7 encodes Smad7, an inhibitory SMAD that provides negative feedback control of TGF-β and BMP signaling by interfering with receptor-mediated phosphorylation of receptor-regulated SMADs and promoting receptor turnover. Through modulation of SMAD-dependent transcription, Smad7 influences epithelial–mesenchymal transition, extracellular matrix remodeling, immune and inflammatory signaling, and cell-cycle regulation. Dysregulated SMAD7 activity has been associated with altered fibrotic responses and inflammatory phenotypes, and context-dependent roles in tumor progression via effects on TGF-β pathway output. As a pathway checkpoint, SMAD7 is frequently studied to dissect signal amplitude and timing in canonical TGF-β/SMAD networks and their cross-talk with MAPK and NF-κB pathways.
Smad7 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the SMAD7 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within SMAD7. 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 SMAD7 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 SMAD7-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.