RGS17 Double Nickase Plasmid (m): sc-425225-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- RGS17 Double Nickase Plasmid (m) 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
- RGS17 Double Nickase Plasmid (m) and RGS17 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Rgs17. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
RGS17 Double Nickase Plasmid (m) | sc-425225-NIC | 20 µg | $410.00 |
Rgs17 encodes regulator of G protein signaling 17 (RGS17), a GAP that accelerates GTP hydrolysis on activated Gα subunits to terminate GPCR signaling. In mouse cells, RGS17 modulates second-messenger dynamics including cAMP/PKA and calcium-dependent signaling, shaping downstream transcriptional and metabolic responses. By tuning GPCR pathway amplitude and duration, it can influence neuronal signaling, secretory processes, and broader signal integration networks. Dysregulated RGS17 activity has been linked in the literature to altered proliferative and survival signaling contexts, making it a useful node for dissecting GPCR-driven phenotypes in disease-relevant models.
RGS17 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Rgs17 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Rgs17. 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 Rgs17 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 Rgs17-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.