Smac Double Nickase Plasmid (m): sc-426096-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Smac 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
- Smac Double Nickase Plasmid (m) and Smac Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Diablo. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Smac Double Nickase Plasmid (m) | sc-426096-NIC | 20 µg | $410.00 |
Mouse Diablo encodes Smac (second mitochondria-derived activator of caspases), a mitochondrial intermembrane space protein released during intrinsic apoptosis. Smac promotes caspase activation by binding inhibitor of apoptosis proteins (IAPs) such as XIAP and cIAPs, thereby relieving IAP-mediated suppression of caspase-3, -7, and -9. Through this IAP–caspase regulatory axis, Smac helps set the threshold for mitochondrial apoptosis downstream of cellular stress, DNA damage, and developmental cues. Dysregulated Smac/IAP signaling is frequently studied in contexts of aberrant cell survival and apoptotic resistance, including oncology and neurodegeneration models.
Smac Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Diablo locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Diablo. 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 Diablo 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 Diablo-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.