PHT2 Double Nickase Plasmid (m): sc-425761-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- PHT2 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
- PHT2 Double Nickase Plasmid (m) and PHT2 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Slc15a3. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
PHT2 Double Nickase Plasmid (m) | sc-425761-NIC | 20 µg | $410.00 |
Slc15a3 encodes the mouse proton-coupled histidine/oligopeptide transporter PHT2, a member of the SLC15 family that contributes to endolysosomal peptide and amino acid handling under acidic pH. PHT2 activity is linked to vesicular trafficking, lysosome-associated nutrient sensing, and antigen processing workflows that influence innate and adaptive immune signaling. By shaping intracellular peptide availability, Slc15a3 can modulate inflammatory responses and stress adaptation pathways in myeloid and epithelial cell contexts. Dysregulation of endolysosomal transport processes involving PHT2 has been associated with immune-driven pathology and altered host defense phenotypes in experimental models.
PHT2 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Slc15a3 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Slc15a3. 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 Slc15a3 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 Slc15a3-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.