uPAR Double Nickase Plasmid (m): sc-422292-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- uPAR 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
- uPAR Double Nickase Plasmid (m) and uPAR Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Plaur. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
uPAR Double Nickase Plasmid (m) | sc-422292-NIC | 20 µg | $410.00 |
Mouse Plaur encodes the urokinase-type plasminogen activator receptor (uPAR), a GPI-anchored cell-surface receptor that localizes proteolysis by binding uPA and coordinating plasmin generation. uPAR integrates extracellular matrix remodeling with cell adhesion and migration through interactions with integrins, vitronectin, and receptor tyrosine kinase signaling, influencing pathways that regulate cytoskeletal dynamics and pericellular protease activity. This axis is central to tissue remodeling, inflammatory cell trafficking, and wound-repair programs, and it is frequently studied in contexts where altered protease networks and stromal signaling reshape microenvironments. Plaur/uPAR biology is therefore relevant to mechanistic research on invasion-like migration, fibrosis-associated remodeling, and immune cell recruitment without implying therapeutic outcomes.
uPAR Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Plaur locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Plaur. 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 Plaur 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 Plaur-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.