TACE/ADAM17 Double Nickase Plasmid (m): sc-418985-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TACE/ADAM17 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
- TACE/ADAM17 Double Nickase Plasmid (m) and TACE/ADAM17 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Adam17. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TACE/ADAM17 Double Nickase Plasmid (m) | sc-418985-NIC | 20 µg | $410.00 |
Mouse Adam17 encodes the transmembrane metalloprotease TACE/ADAM17, a principal sheddase that releases soluble ectodomains of cytokines, growth factors, and receptors. By cleaving substrates such as pro‑TNF, EGFR ligands, and select adhesion molecules, ADAM17 links inflammatory signaling with EGFR/MAPK and NF‑κB–associated pathways, shaping cell communication, proliferation, and stress responses. Its activity intersects with regulated intramembrane proteolysis and membrane trafficking processes that control receptor availability and downstream signaling amplitude. Dysregulated ADAM17-dependent shedding has been implicated in experimental models of inflammatory disease, tissue remodeling, and cancer-related signaling networks, motivating mechanistic studies in immune and epithelial systems.
TACE/ADAM17 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Adam17 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Adam17. 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 Adam17 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 Adam17-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.