CKR-7 Double Nickase Plasmid (h): sc-402150-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CKR-7 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-7 Double Nickase Plasmid (h) and CKR-7 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CCR7. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: CKR-7 Antibody (ELC-Fc): sc-23936
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CKR-7 Double Nickase Plasmid (h) | sc-402150-NIC | 20 µg | $410.00 | |||
CKR-7 Double Nickase Plasmid (h2) | sc-402150-NIC-2 | 20 µg | $410.00 |
CCR7 encodes the chemokine receptor CKR-7, a G protein–coupled receptor that binds CCL19 and CCL21 to regulate leukocyte chemotaxis and tissue homing. CKR-7 signaling engages Gαi-dependent pathways that coordinate actin remodeling, integrin activation, and directional migration, supporting lymphocyte trafficking and dendritic cell localization within secondary lymphoid organs. Through these processes, CCR7 contributes to immune surveillance, lymphoid architecture, and inflammatory cell recruitment. Dysregulated CCR7 expression or signaling has been associated with altered immune cell distribution and has been studied in contexts such as chronic inflammation, autoimmunity, and tumor-immune interactions.
CKR-7 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CCR7 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CCR7. 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 CCR7 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 CCR7-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.