CKR-1 Double Nickase Plasmid (h): sc-402247-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CKR-1 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-1 Double Nickase Plasmid (h) and CKR-1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CCR1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CKR-1 Double Nickase Plasmid (h) | sc-402247-NIC | 20 µg | $410.00 | |||
CKR-1 Double Nickase Plasmid (h2) | sc-402247-NIC-2 | 20 µg | $410.00 |
CCR1 encodes the chemokine receptor CKR-1 (also known as CD191), a seven-transmembrane GPCR that binds CC chemokines such as CCL3, CCL5, CCL7, and CCL23 to regulate leukocyte chemotaxis, adhesion, and tissue infiltration. Ligand engagement activates Gαi-dependent signaling with downstream calcium flux, PI3K/AKT, MAPK, and small GTPase pathways that coordinate integrin activation and directed cell migration. CCR1 activity contributes to inflammatory circuit amplification in myeloid cells and is frequently studied in the context of immune cell trafficking across vascular and tissue barriers. Dysregulated CCR1 signaling has been associated with chronic inflammatory conditions and has been explored in tumor-associated myeloid recruitment and microenvironment remodeling in multiple disease models.
CKR-1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CCR1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CCR1. 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 CCR1 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 CCR1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.