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.
D2DR/Dopamine D2 Receptor Double Nickase Plasmid (m): sc-420053-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- D2DR/Dopamine D2 Receptor 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
- D2DR/Dopamine D2 Receptor Double Nickase Plasmid (m) and D2DR/Dopamine D2 Receptor Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Drd2. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: D2DR/Dopamine D2 Receptor Antibody (B-10): sc-5303
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
D2DR/Dopamine D2 Receptor Double Nickase Plasmid (m) | sc-420053-NIC | 20 µg | $410.00 | |||
D2DR/Dopamine D2 Receptor Double Nickase Plasmid (m2) | sc-420053-NIC-2 | 20 µg | $410.00 |
Drd2 encodes the dopamine D2 receptor (D2DR), a Gi/o-coupled GPCR that inhibits adenylyl cyclase, reduces cAMP/PKA signaling, and modulates ion channel activity to shape neuronal excitability and synaptic transmission. D2DR is highly expressed in striatal medium spiny neurons where it integrates dopaminergic tone with glutamatergic inputs, influencing basal ganglia circuitry, motor control, motivation, and reward learning. Receptor signaling engages pathways including MAPK/ERK and β-arrestin–dependent cascades, linking neurotransmitter dynamics to gene expression programs and plasticity. Altered DRD2 function or expression is associated with neuropsychiatric and neurodegenerative research contexts, including studies of dopaminergic dysregulation, antipsychotic pharmacology, and circuit-level mechanisms of behavior.
D2DR/Dopamine D2 Receptor Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Drd2 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Drd2. 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 Drd2 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 Drd2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.