PI-9 Double Nickase Plasmid (h): sc-404486-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- PI-9 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
- PI-9 Double Nickase Plasmid (h) and PI-9 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting SERPINB9. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: PI-9 Antibody (C-10): sc-390406
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
PI-9 Double Nickase Plasmid (h) | sc-404486-NIC | 20 µg | $410.00 | |||
PI-9 Double Nickase Plasmid (h2) | sc-404486-NIC-2 | 20 µg | $410.00 |
Human SERPINB9 encodes PI-9, an intracellular serine protease inhibitor that primarily neutralizes granzyme B to limit protease-driven apoptosis in cytotoxic lymphocyte interactions. By regulating granzyme B activity in the cytosol, PI-9 influences immune effector pathways, cell survival programs, and proteostasis in contexts where perforin-mediated delivery of granzymes occurs. SERPINB9 expression is prominent in immune cells and tissues exposed to inflammatory stress, where it can modulate susceptibility to cytotoxic attack. Dysregulated PI-9 levels have been associated with altered immune evasion and apoptotic resistance phenotypes reported across inflammation-linked pathologies and cancer biology research.
PI-9 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the SERPINB9 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within SERPINB9. 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 SERPINB9 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 SERPINB9-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.