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.
GR/NR3C1/Glucocorticoid Receptor Double Nickase Plasmid (m): sc-420693-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- GR/NR3C1/Glucocorticoid 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
- GR/NR3C1/Glucocorticoid Receptor Double Nickase Plasmid (m) and GR/NR3C1/Glucocorticoid Receptor Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Nr3c1. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: GR/NR3C1/Glucocorticoid Receptor Antibody (G-5): sc-393232
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
GR/NR3C1/Glucocorticoid Receptor Double Nickase Plasmid (m) | sc-420693-NIC | 20 µg | $410.00 | |||
GR/NR3C1/Glucocorticoid Receptor Double Nickase Plasmid (m2) | sc-420693-NIC-2 | 20 µg | $410.00 |
Mouse Nr3c1 encodes the glucocorticoid receptor (GR/NR3C1), a ligand-activated nuclear receptor that transduces glucocorticoid signals into context-dependent transcriptional programs. Upon hormone binding, GR regulates chromatin accessibility and gene expression through direct glucocorticoid response element binding and tethering to other transcription factors, integrating with NF-κB and AP-1 signaling to shape inflammatory and stress responses. NR3C1 activity influences metabolism, circadian biology, apoptosis, and immune cell differentiation, with dysregulation implicated in altered glucocorticoid sensitivity, neuroendocrine stress phenotypes, and inflammatory disease models. In cancer and metabolic research, GR signaling is studied for its roles in cellular adaptation to stress, treatment response pathways, and tissue-specific transcriptional regulation.
GR/NR3C1/Glucocorticoid Receptor Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Nr3c1 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Nr3c1. 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 Nr3c1 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 Nr3c1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.