MCH-1R Double Nickase Plasmid (m): sc-431527-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- MCH-1R 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
- MCH-1R Double Nickase Plasmid (m) and MCH-1R Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Mchr1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MCH-1R Double Nickase Plasmid (m) | sc-431527-NIC | 20 µg | $410.00 | |||
MCH-1R Double Nickase Plasmid (m2) | sc-431527-NIC-2 | 20 µg | $410.00 |
Mchr1 encodes melanin-concentrating hormone receptor 1 (MCH-1R), a class A GPCR that primarily couples to Gi/o to modulate cAMP signaling, calcium mobilization, and downstream kinase pathways such as MAPK/ERK in neurons. In mouse, MCH-1R is enriched in CNS circuits that integrate energy balance, feeding behavior, arousal, and reward processing, linking receptor activity to neuroendocrine regulation. Altered Mchr1 signaling has been studied in models relevant to obesity, metabolic dysregulation, and neuropsychiatric phenotypes, where changes in synaptic excitability and neuromodulatory tone contribute to systems-level outcomes. As a GPCR node, MCH-1R also provides a tractable entry point for dissecting receptor trafficking, desensitization, and pathway-biased signaling in native cellular contexts.
MCH-1R Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Mchr1 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Mchr1. 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 Mchr1 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 Mchr1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.