OGFR Double Nickase Plasmid (h): sc-407303-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- OGFR 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
- OGFR Double Nickase Plasmid (h) and OGFR Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting OGFR. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
OGFR Double Nickase Plasmid (h) | sc-407303-NIC | 20 µg | $410.00 | |||
OGFR Double Nickase Plasmid (h2) | sc-407303-NIC-2 | 20 µg | $410.00 |
OGFR (opioid growth factor receptor) is a nucleocytoplasmic receptor that binds the endogenous opioid peptide [Met5]-enkephalin (opioid growth factor) and functions as a negative regulator of cell proliferation. Through the OGF–OGFR axis, it modulates cell-cycle progression, commonly linked to control of DNA synthesis and checkpoint regulation, thereby influencing tissue homeostasis and regenerative responses. OGFR expression and signaling have been investigated in contexts of dysregulated growth, including tumor biology and wound repair models, where altered proliferative restraint may contribute to disease-relevant phenotypes. As a conserved regulator of proliferation, OGFR provides a mechanistic entry point for studying how opioid-related signaling interfaces with intracellular pathways that govern cell-cycle control.
OGFR Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the OGFR locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within OGFR. 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 OGFR 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 OGFR-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.