CB2/Cannabinoid Receptor 2/CNR2 Double Nickase Plasmid (m): sc-419723-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CB2/Cannabinoid Receptor 2/CNR2 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
- CB2/Cannabinoid Receptor 2/CNR2 Double Nickase Plasmid (m) and CB2/Cannabinoid Receptor 2/CNR2 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Cnr2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CB2/Cannabinoid Receptor 2/CNR2 Double Nickase Plasmid (m) | sc-419723-NIC | 20 µg | $410.00 | |||
CB2/Cannabinoid Receptor 2/CNR2 Double Nickase Plasmid (m2) | sc-419723-NIC-2 | 20 µg | $410.00 |
Cnr2 encodes cannabinoid receptor 2 (CB2), a Gi/o-coupled GPCR enriched in immune and myeloid lineages that regulates chemotaxis, cytokine release, and inflammatory tone through inhibition of adenylyl cyclase and modulation of MAPK and PI3K/AKT signaling. CB2 activation can influence intracellular Ca²⁺ dynamics and crosstalk with NF-κB-dependent transcriptional programs, shaping innate and adaptive immune responses. In mouse models, Cnr2 function is frequently interrogated in contexts of neuroinflammation, pain processing, metabolic inflammation, and immune cell trafficking, where altered receptor signaling can modify tissue-resident and infiltrating leukocyte phenotypes.
CB2/Cannabinoid Receptor 2/CNR2 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Cnr2 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Cnr2. 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 Cnr2 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 Cnr2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.