RGS7 Double Nickase Plasmid (m): sc-423946-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- RGS7 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
- RGS7 Double Nickase Plasmid (m) and RGS7 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Rgs7. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
RGS7 Double Nickase Plasmid (m) | sc-423946-NIC | 20 µg | $410.00 | |||
RGS7 Double Nickase Plasmid (m2) | sc-423946-NIC-2 | 20 µg | $410.00 |
Rgs7 encodes Regulator of G protein Signaling 7 (RGS7), a neuron-enriched GTPase-activating protein that accelerates Gαi/o and related subunits to terminate GPCR signaling. By shaping the kinetics and amplitude of neurotransmitter-evoked pathways, RGS7 modulates second-messenger outputs including cAMP/PKA and downstream ion channel regulation that influence neuronal excitability and synaptic transmission. RGS7 functions within macromolecular complexes with Gβ5 and membrane anchors such as R7BP to control localization and signaling bias across neural circuits. Dysregulated GPCR signal timing mediated by RGS family proteins is relevant to studies of neurobehavioral phenotypes and circuit-level mechanisms implicated in neurological and psychiatric disease biology.
RGS7 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Rgs7 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Rgs7. 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 Rgs7 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 Rgs7-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.