ChemR23 Double Nickase Plasmid (h): sc-403033-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ChemR23 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
- ChemR23 Double Nickase Plasmid (h) and ChemR23 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CMKLR1. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: ChemR23 Antibody (H-6): sc-398769
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ChemR23 Double Nickase Plasmid (h) | sc-403033-NIC | 20 µg | $410.00 | |||
ChemR23 Double Nickase Plasmid (h2) | sc-403033-NIC-2 | 20 µg | $410.00 |
CMKLR1 encodes ChemR23, a class A G protein–coupled receptor for the chemoattractant chemerin (RARRES2) and pro-resolving lipid ligands such as resolvin E1. ChemR23 signaling engages Gi-dependent pathways including inhibition of adenylyl cyclase, MAPK/ERK activation, intracellular Ca2+ mobilization, and β-arrestin–mediated trafficking, shaping leukocyte chemotaxis and macrophage/dendritic cell responses. In human tissues, CMKLR1 contributes to inflammatory cue sensing and metabolic homeostasis, linking immune cell recruitment with adipose and vascular biology. Dysregulated CMKLR1/ChemR23 activity has been associated with inflammatory disorders and cardiometabolic phenotypes, making it relevant for mechanistic studies of immune–metabolic crosstalk.
ChemR23 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CMKLR1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CMKLR1. 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 CMKLR1 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 CMKLR1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.