PAI-1/SERPINE1 Double Nickase Plasmid (m): sc-422287-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- PAI-1/SERPINE1 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
- PAI-1/SERPINE1 Double Nickase Plasmid (m) and PAI-1/SERPINE1 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Serpine1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
PAI-1/SERPINE1 Double Nickase Plasmid (m) | sc-422287-NIC | 20 µg | $410.00 | |||
PAI-1/SERPINE1 Double Nickase Plasmid (m2) | sc-422287-NIC-2 | 20 µg | $410.00 |
Serpine1 encodes plasminogen activator inhibitor-1 (PAI-1/SERPINE1), a secreted serpin that inhibits tissue- and urokinase-type plasminogen activators to restrain plasmin generation and pericellular proteolysis. Through regulation of fibrinolysis and extracellular matrix remodeling, PAI-1 influences cell adhesion and migration, tissue repair, and inflammatory remodeling, with activity shaped by interactions with vitronectin and endocytic receptors such as LRP1. In mouse systems, altered Serpine1 expression is commonly linked to thrombotic balance, fibrosis, adipose and vascular remodeling, and tumor-associated stromal dynamics, making it a key node connecting protease inhibition to extracellular signaling networks.
PAI-1/SERPINE1 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Serpine1 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Serpine1. 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 Serpine1 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 Serpine1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.