GPRC5B Double Nickase Plasmid (r): sc-437288-NIC
- Target species: rat
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- GPRC5B Double Nickase Plasmid (r) 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
- GPRC5B Double Nickase Plasmid (r) and GPRC5B Double Nickase Plasmid (r2) encode distinct paired gRNA designs targeting . One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
GPRC5B Double Nickase Plasmid (r) | sc-437288-NIC | 20 µg | $410.00 | |||
GPRC5B Double Nickase Plasmid (r2) | sc-437288-NIC-2 | 20 µg | $410.00 |
GPRC5B (G protein-coupled receptor family C group 5 member B) is an orphan GPCR-like membrane protein implicated in regulating receptor trafficking and signal integration at the cell surface. In rat cells, GPRC5B has been linked to modulation of MAPK/ERK and PI3K–AKT signaling dynamics, influencing proliferation, differentiation, and stress-responsive transcriptional programs. Expression and functional studies associate GPRC5B with metabolic and inflammatory phenotypes, including adipocyte biology and insulin signaling, making it a useful target for dissecting pathways underlying obesity-related insulin resistance and cardiometabolic disease mechanisms. Its context-dependent signaling roles also support investigation in neurobiology and epithelial cell homeostasis where GPCR network crosstalk shapes cellular responses.
GPRC5B Double Nickase Plasmid (r) consists of a matched pair of plasmids engineered for high-specificity editing of the locus in rat cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within . 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 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 -disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.