PRL-2 Double Nickase Plasmid (m): sc-422500-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- PRL-2 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
- PRL-2 Double Nickase Plasmid (m) and PRL-2 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Ptp4a2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
PRL-2 Double Nickase Plasmid (m) | sc-422500-NIC | 20 µg | $410.00 |
Mouse Ptp4a2 encodes PRL-2, a prenylated protein tyrosine phosphatase implicated in tuning phosphorylation-dependent signaling at the plasma membrane and endomembranes. PRL-2 activity has been linked to regulation of cell-cycle progression, cytoskeletal remodeling, and migratory behavior through pathways that intersect with MAPK/ERK and PI3K–AKT signaling and downstream control of focal adhesion dynamics. Altered PRL-family phosphatase expression is frequently associated with oncogenic phenotypes, including enhanced proliferation and invasion, making Ptp4a2 a relevant node for mechanistic studies of tumor biology and metastasis-related programs. In immune and developmental contexts, PRL-2 is also studied for its roles in signal integration and tissue homeostasis, supporting its use in pathway mapping and functional genomics.
PRL-2 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Ptp4a2 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Ptp4a2. 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 Ptp4a2 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 Ptp4a2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.