MC1-R Double Nickase Plasmid (m): sc-421583-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- MC1-R 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
- MC1-R Double Nickase Plasmid (m) and MC1-R Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Mc1r. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MC1-R Double Nickase Plasmid (m) | sc-421583-NIC | 20 µg | $410.00 | |||
MC1-R Double Nickase Plasmid (m2) | sc-421583-NIC-2 | 20 µg | $410.00 |
Mouse Mc1r encodes melanocortin 1 receptor (MC1-R), a G protein–coupled receptor that regulates melanocyte differentiation and pigment switching in response to melanocortin ligands such as α-MSH. MC1-R primarily signals through Gαs-driven cAMP/PKA pathways to influence MITF-dependent transcriptional programs, melanin synthesis, and cellular responses to UV-induced stress. Genetic variation or altered expression of MC1-R is linked to changes in coat color and pigmentation phenotypes in mice and is broadly relevant to studies of melanocyte biology and pigment-associated oxidative stress. As a pathway node integrating melanocortin signaling with transcriptional control of melanogenesis, MC1-R provides a tractable target for dissecting GPCR signaling in pigment cells.
MC1-R Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Mc1r locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Mc1r. 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 Mc1r 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 Mc1r-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.