fractalkine Double Nickase Plasmid (m): sc-422853-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- fractalkine 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
- fractalkine Double Nickase Plasmid (m) and fractalkine Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Cx3cl1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
fractalkine Double Nickase Plasmid (m) | sc-422853-NIC | 20 µg | $410.00 | |||
fractalkine Double Nickase Plasmid (m2) | sc-422853-NIC-2 | 20 µg | $410.00 |
Mouse Cx3cl1 encodes fractalkine (CX3CL1), a unique CX3C chemokine presented as both a membrane-tethered adhesion molecule and a soluble chemoattractant after proteolytic shedding. Through binding to CX3CR1, fractalkine regulates leukocyte adhesion, chemotaxis, and survival, integrating inflammatory signaling with cell–cell interactions in vascular, neural, and immune compartments. This axis shapes microglia–neuron communication, monocyte trafficking, and endothelial activation, influencing processes such as synaptic remodeling, tissue surveillance, and cytokine-driven recruitment. Dysregulated CX3CL1/CX3CR1 signaling has been implicated in neuroinflammation, atherosclerosis, and chronic inflammatory states, making Cx3cl1 a useful target for dissecting immune–tissue crosstalk.
fractalkine Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Cx3cl1 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Cx3cl1. 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 Cx3cl1 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 Cx3cl1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.