Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
CB1/Cannabinoid Receptor 1/CNR1 Double Nickase Plasmid (m): sc-419722-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CB1/Cannabinoid Receptor 1/CNR1 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
- CB1/Cannabinoid Receptor 1/CNR1 Double Nickase Plasmid (m) and CB1/Cannabinoid Receptor 1/CNR1 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Cnr1. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: CB1/Cannabinoid Receptor 1/CNR1 Antibody (C-11): sc-518035
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CB1/Cannabinoid Receptor 1/CNR1 Double Nickase Plasmid (m) | sc-419722-NIC | 20 µg | $410.00 |
Cnr1 encodes cannabinoid receptor 1 (CB1/CNR1), a Gi/o-coupled GPCR that responds to endocannabinoids such as anandamide and 2-AG to regulate synaptic transmission and neuronal excitability. CB1 signaling modulates adenylyl cyclase and cAMP/PKA activity, engages MAPK/ERK cascades, and influences Ca²⁺ and K⁺ channel function, shaping neurotransmitter release across multiple brain circuits. In mouse, Cnr1 is central to neuroimmune and metabolic crosstalk, with downstream effects on appetite regulation, reward processing, stress responsiveness, and energy balance. Altered CB1 pathway activity is frequently studied in models of neuropsychiatric phenotypes, pain processing, seizure susceptibility, and obesity-related metabolic dysfunction, supporting broad mechanistic research applications.
CB1/Cannabinoid Receptor 1/CNR1 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Cnr1 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Cnr1. 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 Cnr1 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 Cnr1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.