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.
CKR-3 Double Nickase Plasmid (h): sc-404160-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CKR-3 Double Nickase Plasmid (h) 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
- CKR-3 Double Nickase Plasmid (h) and CKR-3 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CCR3. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: CKR-3 Antibody (5E8): sc-32777
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CKR-3 Double Nickase Plasmid (h) | sc-404160-NIC | 20 µg | $410.00 | |||
CKR-3 Double Nickase Plasmid (h2) | sc-404160-NIC-2 | 20 µg | $410.00 |
CCR3 (CKR-3) is a G protein–coupled chemokine receptor that binds eotaxin family ligands such as CCL11, CCL24, and CCL26 to direct chemotaxis, adhesion, and activation of eosinophils, basophils, and subsets of Th2-polarized immune cells. Upon ligand engagement, CCR3 couples to Gi proteins to regulate intracellular calcium flux, PI3K/AKT and MAPK signaling, cytoskeletal remodeling, and integrin-dependent trafficking across endothelium. CCR3-dependent leukocyte recruitment shapes inflammatory microenvironments at mucosal and airway surfaces and is widely studied in the context of allergic inflammation, asthma, and eosinophilic disorders. Altered CCR3 activity and expression patterns are also examined in chronic inflammatory states and tumor-associated immunity where chemokine gradients influence immune cell infiltration.
CKR-3 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CCR3 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CCR3. 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 CCR3 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 CCR3-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.