GALR1 Double Nickase Plasmid (h): sc-404381-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- GALR1 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
- GALR1 Double Nickase Plasmid (h) and GALR1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting GALR1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
GALR1 Double Nickase Plasmid (h) | sc-404381-NIC | 20 µg | $410.00 | |||
GALR1 Double Nickase Plasmid (h2) | sc-404381-NIC-2 | 20 µg | $410.00 |
GALR1 encodes galanin receptor 1 (GALR1), a Gi/Go-coupled GPCR activated by the neuropeptide galanin that modulates neuronal excitability and neuroendocrine secretion. Upon ligand binding, GALR1 typically inhibits adenylyl cyclase to reduce cAMP/PKA signaling and can engage MAPK and ion channel–linked pathways that shape synaptic transmission. GALR1 signaling contributes to regulation of nociception, feeding behavior, mood-associated circuits, and autonomic function in the central and peripheral nervous systems. Altered GALR1 expression or pathway activity has been investigated in neurological and psychiatric phenotypes and in tumor biology contexts where GPCR signaling and cellular proliferation programs intersect.
GALR1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the GALR1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within GALR1. 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 GALR1 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 GALR1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.