Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Ob-R/Leptin Receptor Double Nickase Plasmid (h): sc-400315-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Ob-R/Leptin Receptor 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
- Ob-R/Leptin Receptor Double Nickase Plasmid (h) and Ob-R/Leptin Receptor Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting LEPR. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: Ob-R/Leptin Receptor Antibody (B-3): sc-8391
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Ob-R/Leptin Receptor Double Nickase Plasmid (h) | sc-400315-NIC | 20 µg | $410.00 | |||
Ob-R/Leptin Receptor Double Nickase Plasmid (h2) | sc-400315-NIC-2 | 20 µg | $410.00 |
LEPR encodes Ob-R, the leptin receptor, a class I cytokine receptor that mediates leptin-dependent control of energy balance, neuroendocrine function, and metabolic homeostasis. Ligand engagement promotes receptor-associated JAK2 activation and downstream STAT3/STAT5 signaling, with additional coupling to PI3K–AKT and MAPK pathways that influence transcriptional programs, cellular excitability, and nutrient sensing. LEPR signaling also interfaces with SOCS3-mediated negative feedback and inflammatory mediators that shape hypothalamic and peripheral responses to adiposity signals. Genetic and functional perturbation of LEPR is closely linked to obesity-related phenotypes and metabolic dysregulation, and is widely studied in adipose, immune, and CNS-relevant models.
Ob-R/Leptin Receptor Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the LEPR locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within LEPR. 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 LEPR 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 LEPR-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.