ERAP2 Double Nickase Plasmid (h): sc-412989-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ERAP2 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
- ERAP2 Double Nickase Plasmid (h) and ERAP2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ERAP2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ERAP2 Double Nickase Plasmid (h) | sc-412989-NIC | 20 µg | $410.00 |
ERAP2 (endoplasmic reticulum aminopeptidase 2) is an ER-resident zinc metallopeptidase that trims N-terminal residues of antigenic peptide precursors for optimal loading onto MHC class I molecules. By shaping the immunopeptidome, ERAP2 contributes to antigen processing and presentation, influencing CD8+ T cell recognition and immune surveillance. Its activity intersects with proteasome/TAP-dependent peptide supply and ER quality-control processes that govern peptide editing prior to surface display. Genetic variation and altered ERAP2 expression have been associated with immune-mediated and inflammatory phenotypes, supporting its use in studies of host–pathogen interactions and HLA-linked disease mechanisms.
ERAP2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ERAP2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ERAP2. 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 ERAP2 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 ERAP2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.