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.
MCR Double Nickase Plasmid (h): sc-400672-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- MCR 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
- MCR Double Nickase Plasmid (h) and MCR Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting NR3C2. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: MCR Antibody (H10E4C9F): sc-53000
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MCR Double Nickase Plasmid (h) | sc-400672-NIC | 20 µg | $410.00 | |||
MCR Double Nickase Plasmid (h2) | sc-400672-NIC-2 | 20 µg | $410.00 |
NR3C2 encodes the mineralocorticoid receptor (MCR), a ligand-activated nuclear receptor that binds mineralocorticoids and glucocorticoids to regulate transcriptional programs controlling epithelial sodium transport, potassium homeostasis, extracellular fluid volume, and blood pressure regulation. Upon hormone binding, MCR translocates to the nucleus and modulates gene expression via hormone response elements and coregulator interactions, intersecting with MAPK signaling and inflammatory transcriptional networks. In the kidney, colon, and cardiovascular tissues, NR3C2 influences ENaC/SGK1-driven ion transport and cellular stress responses, linking receptor activity to electrolyte balance and tissue remodeling. Dysregulation or mutation of NR3C2 is associated with disorders of mineralocorticoid signaling, including salt-wasting phenotypes and altered cardiovascular and renal physiology, supporting its relevance in mechanistic studies of endocrine and cardiorenal pathways.
MCR Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the NR3C2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within NR3C2. 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 NR3C2 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 NR3C2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.