BTN2A2 Double Nickase Plasmid (m): sc-433634-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- BTN2A2 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
- BTN2A2 Double Nickase Plasmid (m) and BTN2A2 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Btn2a2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
BTN2A2 Double Nickase Plasmid (m) | sc-433634-NIC | 20 µg | $410.00 | |||
BTN2A2 Double Nickase Plasmid (m2) | sc-433634-NIC-2 | 20 µg | $410.00 |
Btn2a2 encodes butyrophilin subfamily 2 member A2 (BTN2A2), an immunoregulatory type I transmembrane protein expressed on antigen-presenting cells that modulates T cell activation and peripheral tolerance. BTN2A2 is linked to co-inhibitory signaling that can dampen TCR-driven proliferation and cytokine production, shaping adaptive immune homeostasis. In mouse models, Btn2a2 activity is relevant to pathways controlling immune checkpoint balance, inflammatory responses, and tissue-specific immune regulation. Dysregulated BTN2A2-associated signaling is therefore of interest in studies of autoimmunity, chronic inflammation, and tumor–immune interactions without implying clinical outcomes.
BTN2A2 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Btn2a2 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Btn2a2. 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 Btn2a2 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 Btn2a2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.