CX3CR1 Double Nickase Plasmid (m): sc-419886-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CX3CR1 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
- CX3CR1 Double Nickase Plasmid (m) and CX3CR1 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Cx3cr1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CX3CR1 Double Nickase Plasmid (m) | sc-419886-NIC | 20 µg | $410.00 | |||
CX3CR1 Double Nickase Plasmid (m2) | sc-419886-NIC-2 | 20 µg | $410.00 |
Cx3cr1 encodes the chemokine receptor CX3CR1, a G protein–coupled receptor that binds membrane-tethered and soluble CX3CL1 (fractalkine) to regulate leukocyte adhesion, chemotaxis, and survival. In mouse, CX3CR1 is highly expressed in monocytes/macrophages, dendritic cells, and microglia, shaping immune surveillance, inflammatory trafficking, and neuron–glia communication. Signaling through CX3CR1 modulates pathways including GPCR-mediated calcium flux, PI3K/AKT, and MAPK, influencing cytokine production and phagocytic responses. Altered CX3CR1 activity has been implicated in neuroinflammation and synaptic remodeling as well as cardiovascular and metabolic inflammation, supporting its use in models of tissue injury and chronic inflammatory disease mechanisms.
CX3CR1 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Cx3cr1 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Cx3cr1. 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 Cx3cr1 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 Cx3cr1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.