CKR-6 Double Nickase Plasmid (h): sc-403675-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CKR-6 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-6 Double Nickase Plasmid (h) and CKR-6 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CCR6. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CKR-6 Double Nickase Plasmid (h) | sc-403675-NIC | 20 µg | $410.00 | |||
CKR-6 Double Nickase Plasmid (h2) | sc-403675-NIC-2 | 20 µg | $410.00 |
CCR6 encodes CKR-6, a G protein–coupled chemokine receptor for CCL20 that regulates directional migration of immune cells, including Th17 cells, regulatory T cells, and subsets of dendritic cells. Upon ligand engagement, CCR6 activates heterotrimeric G protein signaling with downstream calcium flux and MAPK/PI3K pathway activity that supports chemotaxis, adhesion, and tissue positioning at epithelial and mucosal sites. CCR6-dependent trafficking contributes to lymphoid tissue organization and inflammatory cell recruitment, linking this axis to immune homeostasis and dysregulated inflammation in autoimmune and chronic inflammatory settings. Aberrant CCR6 signaling has also been investigated in tumor-immune interactions and metastatic behavior through effects on cell motility and microenvironmental recruitment.
CKR-6 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CCR6 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CCR6. 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 CCR6 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 CCR6-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.