TAP2 Double Nickase Plasmid (h): sc-404218-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TAP2 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
- TAP2 Double Nickase Plasmid (h) and TAP2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting TAP2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TAP2 Double Nickase Plasmid (h) | sc-404218-NIC | 20 µg | $410.00 | |||
TAP2 Double Nickase Plasmid (h2) | sc-404218-NIC-2 | 20 µg | $410.00 |
TAP2 (transporter associated with antigen processing 2) encodes an ATP-binding cassette (ABC) transporter subunit that forms a heterodimer with TAP1 to translocate proteasome-derived peptides from the cytosol into the endoplasmic reticulum. This transport step is essential for peptide loading onto MHC class I molecules and subsequent antigen presentation to CD8+ T cells, linking TAP2 to the broader antigen processing and presentation pathway. Altered TAP2 function can remodel the immunopeptidome and affect immune surveillance by changing the quantity and repertoire of surface MHC I–peptide complexes. Genetic defects or regulatory changes in TAP2 have been associated with reduced MHC class I expression and immune evasion phenotypes relevant to infection, inflammatory disorders, and tumor immunobiology.
TAP2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the TAP2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within TAP2. 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 TAP2 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 TAP2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.