AACT Double Nickase Plasmid (h): sc-405262-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- AACT 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
- AACT Double Nickase Plasmid (h) and AACT Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting SERPINA3. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: AACT Antibody (F-10): sc-518261
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
AACT Double Nickase Plasmid (h) | sc-405262-NIC | 20 µg | $410.00 | |||
AACT Double Nickase Plasmid (h2) | sc-405262-NIC-2 | 20 µg | $410.00 |
Human SERPINA3 encodes alpha‑1‑antichymotrypsin (AACT), a secreted serine protease inhibitor that regulates proteolysis by inhibiting chymotrypsin‑like enzymes such as cathepsin G. AACT contributes to extracellular protease–antiprotease balance, shaping inflammatory responses, tissue remodeling, and proteostasis within the acute‑phase reaction. Its expression is modulated by cytokine-driven signaling and is commonly linked to innate immune and stress-responsive programs in hepatocytes and other cell types. Dysregulated SERPINA3/AACT has been associated with chronic inflammation and neurodegeneration-relevant protein homeostasis changes, supporting mechanistic studies of protease regulation in disease contexts.
AACT Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the SERPINA3 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within SERPINA3. 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 SERPINA3 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 SERPINA3-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.