GPR30 Double Nickase Plasmid (h): sc-402502-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- GPR30 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
- GPR30 Double Nickase Plasmid (h) and GPR30 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting GPER1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
GPR30 Double Nickase Plasmid (h) | sc-402502-NIC | 20 µg | $410.00 | |||
GPR30 Double Nickase Plasmid (h2) | sc-402502-NIC-2 | 20 µg | $410.00 |
Human GPER1 encodes GPR30 (GPER), a membrane-associated G protein–coupled estrogen receptor that mediates rapid, non-genomic estrogen signaling. Upon activation, GPR30 modulates second-messenger pathways including cAMP/PKA, intracellular calcium mobilization, and MAPK/ERK and PI3K/AKT cascades, influencing cell proliferation, survival, migration, and inflammatory responses. GPER1 activity intersects with EGFR transactivation and broader steroid hormone signaling networks, shaping transcriptional programs through downstream kinase signaling. Dysregulated GPER1/GPR30 signaling has been implicated in hormone-responsive cancers, cardiovascular and metabolic phenotypes, and immune-related processes, making it a relevant target for mechanistic studies in cell signaling and disease models.
GPR30 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the GPER1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within GPER1. 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 GPER1 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 GPER1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.