AdipoR1 Double Nickase Plasmid (h): sc-400995-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- AdipoR1 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
- AdipoR1 Double Nickase Plasmid (h) and AdipoR1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ADIPOR1. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: AdipoR1 Antibody (D-9): sc-518030
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
AdipoR1 Double Nickase Plasmid (h) | sc-400995-NIC | 20 µg | $410.00 | |||
AdipoR1 Double Nickase Plasmid (h2) | sc-400995-NIC-2 | 20 µg | $410.00 |
ADIPOR1 encodes adiponectin receptor 1 (AdipoR1), a seven-transmembrane receptor that mediates adiponectin signaling to regulate cellular energy homeostasis. AdipoR1 activation promotes AMP-activated protein kinase (AMPK) and PPARα-dependent pathways, influencing fatty acid oxidation, glucose uptake, mitochondrial function, and cellular stress responses. In human tissues, ADIPOR1 is broadly expressed and contributes to metabolic adaptation in muscle and other energy-demanding cells. Dysregulation of ADIPOR1 signaling has been associated with insulin resistance, obesity-related metabolic dysfunction, and altered inflammatory signaling, making it a useful target for mechanistic studies of metabolic disease pathways.
AdipoR1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ADIPOR1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ADIPOR1. 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 ADIPOR1 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 ADIPOR1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.